NEUROLOGY Flashcards
1
Q
An acute, frequently severe, and fulminant polyradiculoneuropathy that is autoimmune in nature
A
GBS
2
Q
Manifests as a rapidly evolving areflexic motor paralysis with or without sensory disturbance.
A
GBS
3
Q
Usual pattern of paralysis in GBS
A
ascending paralysis that may be first noticed as rubbery legs
legs > arms
facial diparesis – 50%
bulbar weakness
4
Q
T or F. Fever and constitutional symptoms are usually present at the onset of GBS
A
False. Fever and constitutional symptoms are absent at the onset and, if present, cast doubt on the diagnosis
5
Q
T or F. Bladder dysfunction is a usual presentation of GBS
A
False. Bladder dysfunction may occur in severe cases but is usually transient. If bladder dysfunction is a prominent feature and comes early in the course or there is a sensory level on examination, diagnostic possibilities other than GBS should be considered, particularly spinal cord disease
6
Q
T or F. Autonomic involvement is common in GBS
A
True. The usual manifestations are loss of vasomotor control with wide fluctuations in blood pressure, postural hypotension, and cardiac dysrhythmias
7
Q
Description of pain in GBS
A
Deep aching pain may be present in weakened muscles that patients liken to having overexercised the previous day
8
Q
The most common variant of GBS
A
acute inflammatory demyelinating polyneuropathy (AIDP)
9
Q
2 axonal variants of GBS that are often clinically severe
A
Acute motor axonal neuropathy (AMAN)
Acute motor sensory axonal neuropathy (AMSAN)
10
Q
GBS variant which presents as rapidly evolving ataxia and areflexia of limbs without weakness, and ophthalmoplegia, often with pupillary paralysis.
A
Miller Fisher syndrome
accounts for ~5% of all cases
11
Q
MFS is strongly associated with antibodies to the
A
ganglioside GQ1b
found in >90% of patients with MFS
12
Q
Approximately ____ of cases of GBS occur 1–3 weeks after an acute infectious process, usually respiratory or gastrointestinal.
A
70%
13
Q
T or F. Some vaccines may increase the risk of GBS.
A
True. The swine influenza vaccine, administered widely in the United States in 1976, is the most notable example
14
Q
Aside from prior infection and vaccinations, risk of GBS is also increased in these group of patients (3)
A
- lymphoma (including Hodgkin’s disease)
- HIV-seropositive individuals
- Systemic lupus erythematosus (SLE)
15
Q
These antibodies are common in GBS (20–50% of cases), particularly in AMAN and AMSAN and in those cases preceded by C. jejuni infection
A
Antiganglioside antibodies, most frequently to GM1
16
Q
In the demyelinating forms of GBS, the basis for flaccid paralysis and sensory disturbance is
A
conduction block
axonal connections remain intact
17
Q
______ after the first motor symptoms, it is not known whether immunotherapy is still effective for GBS
A
~2 weeks
If the patient has already reached the plateau stage, then treatment probably is no longer indicated, unless the patient has severe motor weakness and one cannot exclude the possibility that an immunologic attack is still ongoing
18
Q
Management of GBS (2)
A
High dose IVIg
Plasmapheresis
Equally effective
19
Q
Dose of IVIg in GBS
A
five daily infusions for a total dose of 2 g/kg body weight
20
Q
Dose of plasmapheresis in GBS
A
~40–50 mL/kg PE 4–5 times over 7–10 days
21
Q
T or F. Glucocorticoids is used as treatment in GBS.
A
False. Glucocorticoids have not been found to be effective in GBS .
22
Q
Approximately ____ of patients with GBS achieve a full functional recovery within several months to a year, although minor findings on examination (such as areflexia) may persist and patients often complain of continued symptoms, including fatigue
A
85%
23
Q
Mortality rate of GBS in an optimal setting
A
< 5%
24
Q
T or F. CIDP responds to glucocorticoids
A
True
25
Criteria used in diagnosis of GBS and MFS
Brighton criteria
26
T or F. Virtually every possible type of focal neurologic disturbance has been reported in viral encephalitis
True
27
An inflammation of the brain caused either by infection or from a primary autoimmune process
Encephalitis
28
Most commonly identified viruses causing sporadic cases of acute encephalitis in immunocompetent patients
Herpesviruses
HSV, VZV, and EBV
29
A member of the Paramyxoviridae family that caused outbreak of encephalitis in Southest Asia
Nipah virus
30
T or F. Not all patients with suspected viral encephalitis should have CSF examination
False. Should be performed in all patients with suspected viral encephalitis unless contraindicated by the presence of severely increased intracranial pressure (ICP).
31
In CSF examination, how many mL of CSF must be collected?
at least 20 mL
5–10 mL stored frozen for later studies as needed
32
Atypical lymphocytes in the CSF is seen what infection?
EBV
33
RBCs in the CSF (>500/μL) is seen in 20% of patients with nontraumatic tap. This is most often caused by
HSV
Hemorrhagic encephalitis
34
Primary diagnostic test for CNS infections caused by CMV, EBV, HHV-6, and enteroviruses
CSF PCR
35
Nearly 80% of patient with HSV encephalitis will have abnormalities in the _____ lobe in MRI
Temporal
10% has abnormalities in the extratemporal regions
10% - normal MRI
36
Periodic, stereotyped, sharp-and-slow complexes originating in one or both temporal lobes and repeating at regular intervals of 2-3 s is a distinctive EEG pattern of
HSV encephalitis
37
Primary amebic meningoencephalitis cause
Naegleria fowleri
38
Causes of subacute or chronic granulomatous amebic meningoencephalitis
Acanthamoeba and Balamuthia
39
The major diagnostic challenge in management of viral encephalitis
To distinguish HSV from other viruses that cause encephalitis
Important to distinguish because HSV can be treated effectively with antiviral therapy
40
Empiric treatment of viral encephalitis with dose
Acyclovir 10 mg/kg IV every 8 h (30 mg/kg per day total dose) for 21 days
Each dose should be infused slowly over 1 h
Discontinued if proven to be not HSV encephalitis but may be continued with severe VZV or EBV
41
Treatment of CMV-related CNS infections
Ganciclovir and foscarnet
Alternative: cidofovir
Valganciclovir – oral drug
42
Dose of ganciclovir in CMV-related CNS infections
* Induction therapy dose: 5 mg/kg q12h IV at a constant rate over 1 h
* Maintenance therapy: 5 mg/kg per day for an indefinite period
43
Multifocal areas of demyelination of varying size distributed throughout the brain but sparing the spinal cord and optic nerves. This is seen in what condition
Progressive Multifocal Leukoencephalopathy
44
Most common visual defect in Progressive Multifocal Leukoencephalopathy
Homonymous hemianopia
45
80% of Progressive Multifocal Leukoencephalopathy patients has this comorbid
AIDS
46
5-HT2a receptor antagonist that may have potential beneficial effects because it may inhibit binding of JCV to its receptor on oligodendrocytes in patients with PML
Mirtazapine
47
A rare, chronic, progressive demyelinating disease of the CNS associated with a chronic nonpermissive infection of brain tissue with measles virus
Subacute sclerosing panencephalitis (SSPE)
Some 85% of patients are between 5 and 15 years old at diagnosis
48
Extremely rare disorder that primarily affects males with congenital rubella syndrome
Progressive Rubella Panencephalitis
49
The best test for WNV encephalitis is the
CSF IgM antibody test
50
A neuromuscular junction (NMJ) disorder characterized by weakness and fatigability of skeletal muscles
Myasthenia gravis (MG)
51
Decrease in the number of available acetylcholine receptors (AChRs) at NMJs due to an antibody-mediated autoimmune attack
Myasthenia gravis (MG)
52
Binding subunit of AChR
α subunit
AChR has 5 subunits: 2α, 1β, 1δ, 1γ, or ε
53
The amount of the ACh released per pulse normally declines on repeated activity. This phenomenon is called
Presynaptic rundown
54
Decreased efficiency of the neuromuscular transmission plus the normal rundown results in the activation of fewer and fewer muscle fibers by successive nerve impulses hence increasing weakness causes this clinical manifestation
Myasthenic fatigue
55
Antibodies that are present in 10% of patients with MG
Anti- muscle-specific kinase (MuSK)
56
Thymus is abnormal in ___ of patients with MG
~75%
57
Most common thymic abnormality in MG
Hyperplasia – 65%
Thymoma in 10%
58
Muscle-like cells in the thymus that may serve as a source of autoantigen and trigger the autoimmune reaction within the thymus gland in MG patients
Myoid cells
59
Peak incidence of MG in men and women
* Women in their 20s and 30s
* Men in their 50s and 60s
Women > men – 3:2
60
Cardinal features of MG (2)
* Weakness
| * Fatigability
61
Characteristic of weakness in MG
Weakness increases during repeated use or late in the day and may improve following rest or sleep
62
Common initial complaints in MG
Diplopia and ptosis
63
Facial weakness in MG is described as
“snarling” expression when patient attempts to smile
64
Characteristic of speech in MG
Nasal speech - weakness of the palate
| Dysarthric “mushy” quality of voice – due to tongue weakness
65
Bulbar weakness is prominent in what subset of MG patients
MuSK antibody-positive
66
T or F. If MG isrestricted to EOM for 1 year, it is likely that weakness will not be generalized
False. 3 years.
Ocular MG
67
Effect of Ice Pack Test in MG
Improvement of ptosis
Less depletion of the AChR in the cold and reduced activity of AChE
68
Antibodies that is detected in ~85% in all MG patents
Anti AChR antibodies
69
Autoantibodies associated with MG (5)
1. Anti AChR antibodies
2. Anti MuSK antibodies
3. Anti LRP4 antibodies
4. Anti Agrin Antibodies
5. Anti-striated muscle antibodies
70
Anti-AChE medication should be stopped _____ before electrodiagnostic testing
6-12 h
71
Normal response in electrodiagnostic testing
AP does not change by >10%
72
MG response in electrodiagnostic testing
Rapid reduction of >10% in the amplitude of the evoked responses
73
Anticholinesterase that is most commonly used for diagnostic testing
Endrophonium
* Rapid onset – 30 s
* Short duration – 5 mins
74
Dose of edrophonium in anticholinesterase test
Initial IV dose of 2mg endrophonium
| Additional 8mg IV may be given if no response
75
Positive response in anticholinesterase test for MG
Improvement of weakness
76
In patients with adverse effects during anticholinesterase test, what may be given?
Atropine 0.6 mg
ADRs: nausea, diarrhea, salivation, fasciculations, and rarely, syncope or bradycardia
77
Anticholinesterase test may be false positive for MG if with this condition
ALS
78
Rare heterogenous group of disorders of the NMJ that are not autoimmune and is due to genetic mutations in which virtually all component of the NMJ may be affected
Non-autoimmune congenital myasthenia
79
Most common mutation in AChR in congenital myasthenia is seen in what subunit?
Mutation of ε subunit of the AChR - ~50% of the cases
80
Non-autoimmune congenital myasthenia that worsens with AChE inhibitors (3)
1. Slow channel syndrome
2. AChE deficiency
3. DOK-7 related CMS
81
Drug-induced MG may be caused by (2)
1. Penicillamine
| 2. Checkpoint inhibitors for cancer
82
Presynaptic disorder of the NMJ that mostly involves the proximal muscles of the lower limbs
Lambert-Eaton Myasthenic Syndrome (LEMS)
83
Difference of Lambert-Eaton Myasthenic Syndrome (LEMS) with MG
Have depressed or absent reflexes and experience autonomic changes such as dry mouth and impotence
84
Lambert-Eaton Myasthenic Syndrome (LEMS) is caused by autoantibodies directed against the
P/Q-type Ca channels at the motor nerve terminals
Impair the release of ACh from nerve terminals
85
Most common cancer associated with Lambert-Eaton Myasthenic Syndrome (LEMS)
Small-cell Lung Cancer
86
Treatment of Lambert-Eaton Myasthenic Syndrome (4)
Plasmapheresis
Immunotherapy
3,4 DAP
Pyridostigmine
87
Treatment of LEMS that blocks K channels prolonging depolarization of the motor nerve terminals, thus enhancing ACh release
3,4 DAP
88
Myasthenia-like fatigue syndrome without an organic basis
Neurasthenia
Subjective symptoms of weakness and fatigue
Muscle testing reveals “give-away weakness”
89
T or F. Thyroid function test must be obtained in all patients suspected to have MG
True. Hyperthyroidism or hypothyroidism may be present in MG patients or may aggravate myasthenic weakness
90
Most common autoimmune disorders that coexist with MG (2)
SLE and RA
91
Most widely used anticholinesterase drugs for MG
Pyridostigmine
92
Dose of pyridostigmine for MG
Initial dose: 30-60 mg 3-4 x a day
| Max dose: 300 mg daily
93
T or F. Pyridostigmine is less beneficial for anti-MuSK MG
True. May actually worsen
94
Immunosuppressive treatment for MG if immediate improvement is essential
IVIg or plasmapheresis
95
Intermediate term immunosuppressive treatment for MG
glucocorticoids and cyclosporine or tacrolimus (provides improvement within 1-3 months)
96
Long term immunosuppressive treatment for MG
azathioprine and mycophenolate mofetil
97
Immunotherapy for MG that inhibits purine synthesis by the de novo pathway
Mycophenolate mofetil
Lymphocyte only have the de novo pathway and not the salvage pathway that is present in other cells
98
Azathioprine must not be used with this drug because it may cause severe bone marrow suppression due to common degradation pathway
Allopurinol
99
Calcineurin inhibitors used as immunosuppressive therapy for MG (2)
Cyclosporine
| Tacrolimus
100
Monoclonal antibody that is effective in MuSK antbody positive MG
Rituximab
101
Treatment for rare refractory MG patients that reboots the immune system
High-dose cyclophosphamide
102
Dose of plasmapheresis in MG
5 exchanges (3-4 L per exchange) for 10-14 days
Short-term reduction in anti-AChR antibodies
103
Dose of IVIg in MG
2g/kg for >2-5 days
Short-term reduction in anti-AChR antibodies
104
An exacerbation of weakness sufficient to endanger life with ventilatory failure caused by diaphragmatic and intercostal muscle weakness
Myasthenic crisis
105
Deterioration in MG due to excessive AChE inhibitors
Cholinergic crisis
106
Most common cause of crisis in MG
Intercurrent infection
107
Subset of MG that does not typically experience crisis but are more difficult to treat
Anti MuSK positive MG
108
Antibiotics that may exacerbate MG (3)
Aminoglycosides
Macrolides
Quinolones
109
Most common causes of SAH (2)
* Head trauma
| * Rupture of a saccular aneurysm
110
Mortality rate of SAH secondary to saccular “berry” aneurysm over the next month after the rupture:
45% (for patients who arrive alive at hospital)
111
Of those who survive rupture of saccular aneurysm, more than half are left with major neurologic deficits as a result of (3)
* Initial hemorrhage
* Cerebral vasospasm with infarction
* Hydrocephalus
112
If saccular aneurysm is not obliterated, rate of rebleeding in the first 2 weeks
20%
113
If saccular aneurysm is not obliterated, rate of rebleeding in the first month
30%
114
If saccular aneurysm is not obliterated, rate of rebleeding per year
3%
115
Berry aneurysms <10 mm in size has a ____ annual risk of rupture
0.1%
116
Berry aneurysms >10 mm in size has a ____ annual risk of rupture
~0.5–1%
117
Location of saccular aneurysm with the highest risk of bleeding
Basilar bifurcation aneurysms
118
Giant saccular aneurysms is ____ in diameter
>2.5 cm
119
3 most common locations of giant saccular aneurysms
* Terminal internal carotid artery
* Middle cerebral artery (MCA) bifurcation
* Top of the basilar artery
120
Usual location of mycotic aneurysm
distal to the first bifurcation of major arteries of the circle of Willis
121
This result from infected emboli due to bacterial endocarditis causing septic degeneration of arteries and subsequent dilation and rupture
Mycotic aneurysms
122
Usual locations of berry aneurysm
bifurcations of the large- to medium-sized intracranial arteries
123
Approximately 85% of saccular aneurysms occur in the _____ circulation
Anterior
Mostly on the circle of Willis
124
About ____ of patients have multiple brain aneurysms
20%
Many at mirror sites bilaterally
125
Features of aneurysm that are important factors in planning neurosurgical obliteration or endovascular embolization (2)
Length of the neck and size of the dome
126
Part of saccular aneurysm that is the most often site of rupture
Dome
Wall thins
127
Factors for greater risk of rupture of saccular aneurysm (3)
* > 7 mm in diameter
* At the top of the basilar artery
* At the origin of the posterior communicating artery
128
Presenting complaint in ~45% of cases of rupture of aneurysm
Severe headache associated with exertion
“the worst headache of my life”
129
The most important characteristic of the headache of ruptured aneurysm
Sudden onset
Generalized headache, often with neck stiffness and vomiting
130
The hallmark of brain aneurysmal rupture
Sudden headache in the absence of focal neurologic symptoms
131
Bleeding of aneurysm in this sites will cause hemiparesis, aphasia, and mental slowness (abulia) (2)
1. Anterior communicating artery
| 2. MCA bifurcation aneurysms
132
Aneurysm in this sites will cause third cranial nerve palsy (2)
1. junction of the posterior communicating artery
| 2. internal carotid artery
133
Aneurysm in this site will cause 6th cranial nerve palsy
cavernous sinus
134
Aneurysm in this site will cause visual field defects (2)
1. supraclinoid carotid
| 2. anterior cerebral artery (ACA) aneurysm
135
Aneurysm in this site will cause occipital and posterior cervical pain (2)
1. posterior inferior cerebellar artery
| 2. anterior inferior cerebellar artery
136
Aneurysm in this site will cause pain in or behind the eye and in the low temple (2)
Expanding MCA aneurysm
137
A variant of migraine that simulates an SAH
Thunderclap headache
A definitive workup for aneurysm or other intracranial pathology is required
138
Small ruptures of brain aneurysm and leaks of blood into the subarachnoid space
Sentinel bleeds
139
Grade the initial clinical manifestations of SAH
Hunt-Hess
Or World Federation of Neurosurgical classification schemes
140
4 major causes of delayed neurologic deficits in aneurysmal rupture
1. Rerupture
2. Hydrocephalus
3. Delayed cerebral ischemia
4. Hyponatremia
141
Incidence of rerupture of an untreated aneurysm in the first month following SAH is ____, with the peak in the first ____
~30%,
7 days
142
Narrowing of the arteries at the base of the brain following SAH
Vasospasm
143
Delayed cerebral ischemia in aneurysmal rupture is secondary to
Vasospasm
May cause symptomatic ischemia and infarction in ~30%
Result from direct effects of clotted blood and its breakdown products on the arteries within the subarachnoid space
The more blood that surrounds the arteries, the greater chance of symptomatic vasospasm
144
Major cause of delayed morbidity and death in aneurysmal rupture
Vasospasm
Often preceded by a decline in mental status
145
Vasospasm appear ____ after the SAH, most often at _____
4-14 days
7 days
146
Cerebral salt-wasting syndrome in SAH is due to (2)
Natriuresis
Volume depletion
hyponatremia and hypovolemia
147
Laboratory hallmark of aneurysmal rupture
blood in the CSF
148
Based on high-quality non-contrast CT scan, high incidence of symptomatic vasospasm in MCA and ACA (2)
* Subarachnoid clots >5 x 3 mm in the basal cisterns
| * Layers of blood > 1 mm thick in cerebral fissures
149
Yellow spinal fluid in SAH
Xanthochromic spinal fluid
Due to lysis of RBCs and subsequent conversion of hemoglobin to bilirubin
within 6-12 hrs
150
ECG changes sec to intracranial hemorrhage (4)
1. Prolonged QRS
2. Increased QT
3. Prominent “peaked” T wave
4. Deeply inverted symmetric T waves
151
Aneurysmal repair may be via (2)
1. Clipping of aneurysm (metal clip across the aneurysmal neck)
2. Endovascular coiling (Placing of platinum coils or other embolic material within the aneurysm)
152
If patient with SAH is alert, systolic BP must be maintained
below 160 mmHg
153
If patient with SAH has depressed sensorium, systolic BP must be maintained based on
CPP targeted at 60-70 mmHg
154
Management of vasospasm and delayed cerebral ischemia in aneurysmal rupture
Nimodipine 60 mg PO every 4 hours
155
This drug prevent ischemic injury rather than reducing the risk of vasospasm in aneurysmal rupture
Nimodipine
Ca-channel antagonist
156
Pharmacologic vasodilators that may be used in vasospasm of aneurysmal rupture (2)
Verapamil and nicardipine
157
For DVT prophylaxis, unfractionated heparin can be initiated within ____following coiling or clipping
1–2 days
158
T or F. Seizure is uncommon at the onset of aneurysm rupture
True
Quivering, jerking, and extensor posturing – may be related to increased ICP and not the seizure
159
Why is free water restriction contraindicated in management of SAH?
May cause hypovolemia and hypotension cerebral ischemia
160
Hunt and Hess I
Mild headache, normal mental status, no cranial nerve or motor findings
161
Hunt and Hess II
Severe headache, normal mental status, may have cranial nerve deficit
162
Hunt and Hess III
Somnolent, confused, may have cranial nerve or mild motor deficit
163
Hunt and Hess IV
Stupor, moderate to severe motor deficit, may have intermittent reflex posturing
164
Hunt and Hess V
Coma, reflex posturing or flaccid
165
The most common form of suppurative CNS infection
Acute meningitis
166
Most common organisms causing community-acquired bacterial meningitis (in order)(5)
```
Streptococcus pneumoniae (~50%)
Neisseria meningitidis (~25%)
Group B streptococci (~15%)
Listeria monocytogenes (~10%)
Haemophilus influenzae type b (<10%)
```
167
Causative organism of recurring epidemics of meningitis every 8–12 years
Neisseria meningitidis
168
The most common cause of meningitis in adults >20 years of age
S. pneumoniae
169
Most important risk factor in acute meningitis caused by S. pneumoniae
Pneumococcal pneumonia
170
Why is there incidence of meningitis caused by N meningitidis even in patients vaccinated against the organism?
Usual vaccine does not contain serogroup B (responsible for 1/3 of cases of meningococcal disease)
Serogroup B meningococcal (MenB) vaccine must be given to aged 16-23 y.o.
171
Important clue to the diagnosis of meningococcal infection
Petechial or purpuric skin lesions
172
Initial infection in acute meningitis caused by N. meningitidis
Nasopharyngeal colonization
173
Gram-negative bacilli cause meningitis in individuals with
chronic and debilitating diseases
diabetes, cirrhosis, or alcoholism and in those with chronic urinary tract infection
174
Previously responsible for meningitis predominantly in neonates
Group B Streptococcus (i.e. Streptococcus agalactiae)
Increasing frequency in aged >50 years
175
Causative agent of meningitis acquired by ingesting contaminated foods (coleslaw, milk, soft cheeses, and several types of “ready-to-eat” foods)
L. monocytogenes
176
Important causes of meningitis that occurs following invasive neurosurgical procedures (i.e. shunting procedures) or as a complication of the use of subcutaneous Ommaya reservoirs for administration of intrathecal chemotherapy
S. aureus and coagulase-negative staphylococci
177
T or F. Many of the neurologic manifestations and complications of bacterial meningitis result from the direct bacteria-induced tissue injury
False.
Many of the neurologic manifestations and complications of bacterial meningitis result from the immune response to the invading pathogen rather than from direct bacteria-induced tissue injury
178
These 2 cytokines act synergistically to increase the permeability of the blood-brain barrier
TNF-α and IL-1β
179
Classic clinical triad of acute meningitis
* Fever
* Headache
* Nuchal rigidity
180
Pathognomonic sign of meningeal irritation
Nuchal rigidity
181
Decreased level of consciousness occurs in ____ of patients with meningitis
>75%
lethargy to coma
182
Elicited with the patient in the supine position and thigh is flexed on the abdomen, with the knee flexed. Positive response is noted when patient’s attempt to passively extend the knee elicit pain
Kernig’s sign
183
Elicited with the patient in the supine position and is positive when passive flexion of the neck results in spontaneous flexion of the hips and knees
Brudzinski’s sign
184
Major cause of obtundation and coma in acute meningitis
Raised ICP
185
More than 90% of patients with acute meningitis will have a CSF opening pressure
>180 mmH2O
186
Cushing reflex is a sign of
Raised ICP
187
Cushing reflex (3)
* Bradycardia
* Hypertension
* Irregular respirations
188
The most disastrous complication of increased ICP
Cerebral herniation
189
CSF analysis is bacterial meningitis in terms of:
```
Cell count and differential
Glucose
CSF/serum glucose
Protein
Opening pressure
```
```
Cell count and differential: 10-10000 cells/ neutrophilic predominance
Glucose: <2.2 mmol/L (<40 mg/dl)
CSF/serum glucose: <0.4
Protein: 0.45 g/L (>45 mg/dL)
Opening pressure: >180 mmH2O
```
190
A rapid diagnostic test for the detection of gram-negative endotoxin in CSF and thus for making a diagnosis of gram-negative bacterial meningitis
Limulus amebocyte lysate assay
191
Preferred imaging for acute meningitis
MRI
Diffuse meningeal enhancement – not diagnostic of meningitis but occurs in any CNS disease associated with increased blood-brain barrier permeability
192
Rocky Mountain spotted fever (RMSF) is caused by the bacteria
Rickettsia rickettsia
transmitted by a tick bite
193
Characteristic rash within 96 h of the onset of symptoms is initially a diffuse erythematous maculopapular rash that may be difficult to distinguish from that of meningococcemia, which progresses to a petechial rash, then to a purpuric rash, and if untreated, to skin necrosis or gangrene
Rocky Mountain spotted fever (RMSF)
194
Goal in empirical antimicrobial therapy of acute meningitis
antibiotic therapy within 60 min of a patient’s arrival in the emergency room
195
Empiric antimicrobial therapy for hospital-acquired meningitis (usually following neurosurgical procedures):
Vancomycin + ceftazidime/meropenem
Staphylococci and gram-negative organisms including P. aeruginosa are the most common etiologic organisms
196
Antibiotic of choice for meningococcal meningitis
Pen G
7-day course – if uncomplicated
197
Chemoprophylaxis for meningococcal meningitis
Rifampin 600 mg q12h for 2 days in adults
Alternative: azithromycin 500 mg single dose or ceftriaxone 250 mg IM single dose
Close contacts: contact with oropharyngeal secretions (e.g. kissing or by sharing toys, beverages, or cigarettes)
198
Antibiotic of choice for pneumococcal meningitis
Cephalosporin (ceftriaxone, cefotaxime, or cefepime) + vancomycin
2-week therapy
199
Ideally, when must LP be repeated after the initiation of antimicrobial therapy to document sterilization of CSF
24-36 h
Failure to strerilize CSF – presumptive evidence of antibiotic resistance
200
Antibiotic of choice for Listeria meningitis
Ampicillin for at least 3 weeks
Gentamicin is added in critically ill patients
2 mg/kg loading dose, then 7.5 mg/kg per day given every 8 h and adjusted for serum levels and renal function
Alternative for penicillin-allergic patients: Co-trimoxazole (trim 10–20 mg/kg per day and sulfa 50–100 mg/kg per day) given every 6 h
201
The drug of choice for MRSA and for patients allergic to penicillin
Vancomycin
202
Antibiotic of choice for gram-negative bacillary meningitis
Third-generation cephalosporins for 3 weeks
203
Dexamethasone exerts its beneficial effect in acute meningitis therapy by (3)
* Inhibiting the synthesis of IL-1β and TNF-α at the level of mRNA
* Decreasing CSF outflow resistance
* Stabilizing the blood-brain barrier
204
In acute meningitis management, Dexamethason must be given ____ before antibiotic therapy. Give the rationale.
20 min
Dexamethasone inhibits the production of TNF-α by macrophages and microglia only if it is administered before these cells are activated by endotoxin. It does not alter TNF-α production once it has been induced
205
Dose of dexamethasone in acute meningitis
10 mg IV 15-20 mins before 1st dose of antimicrobial agent, then q6h for 4 days
206
Management of increased ICP (4)
* Elevation of the patient’s head to 30–45°
* Intubation
* Hyperventilation (PaCO2 25–30 mmHg)
* Mannitol
207
Mortality rates for acute meningitis caused by H. influenzae, N. meningitidis, or group B streptococci
3–7%
208
Mortality rates for acute meningitis caused by L. monocytogenes
15%
209
Mortality rates for acute meningitis caused by S. pneumoniae
20%
210
CSF values that is predictive of increased mortality and poorer prognosis in acute meningitis (2):
1. Decreased CSF glucose concentration (<2.2 mmol/L [<40 mg/dL])
2. Markedly increased CSF protein concentration (>3 g/L [> 300 mg/dL])
211
Characteristic of headache in viral meningitis
frontal or retroorbital
| Associated with photophobia and pain on moving the eyes
212
Which HSV more commonly cause the viral meningitis?
HSV 2 > HSV 1
HSV-1 – 90% of HSV encephalitis
213
Most important laboratory test in the diagnosis of viral meningitis
CSF Examination
214
CSF analysis is viral meningitis in terms of:
Cell count and differential
Glucose
Protein
Opening pressure
Cell count and differential: 25-500/μL; lymphocytic predominance
Glucose: normal
Protein: normal or sl. elevated
Opening pressure: 100-350 mmH2O
215
The single most important method for diagnosing CNS viral infections
PCR amplification of viral nucleic acid
216
Diagnostic procedure of choice for both enteroviral and HSV infections of the CNS
CSF PCR
217
Most common cause of viral meningitis (>85% of cases)
Enteroviruses
218
Viral infection that caused large epidemics of neurologic disease in Southeast Asia
Enterovirus 71
219
Major cause of viral meningitis in adults
HSV meningitis
220
Second most common cause of viral mengitis
HSV meningitis
221
Most common cause of recurrent viral or “aseptic” meningitis
HSV meningitis
222
Presence of atypical lymphocytes in the CSF or peripheral blood
EBV meningitis
223
Cranial nerve palsies is more common in what viral meningitis as compared with other viral infections
HIV meningitis
224
Most commonly involved cranial nerves in HIV meningitis (3)
V, VII, or VIII
225
Meningitis associated with history of exposure to house mice (Mus musculus), pet or laboratory rodents (e.g., hamsters, rats, mice), or their excreta; some patients have an associated rash, pulmonary infiltrates, alopecia, parotitis, orchitis, or myopericarditis
LCMV infection
226
Most common pathogen causing fungal meningitis
C. neoformans
227
Most frequently involved cranial nerves in neurosyphilis (2)
Cranial nerves VII and VIII
228
Most common causes of subacute meningitis (5)
1. M. tuberculosis
2. C. neoformans
3. H. capsulatum
4. C. immitis
5. T. pallidum
229
The combination of unrelenting headache, stiff neck, fatigue, night sweats, and fever with a CSF lymphocytic pleocytosis and a mildly decreased glucose concentration is highly suspicious for
tuberculous meningitis
230
In the LP procedure, this is the best tube to send for a smear for acid-fast bacilli (AFB)
Last tube
231
Positive AFB smears is seen in only ____ of cases of tuberculous meningitis in adults
10–40%
232
The gold standard to make the diagnosis of tuberculous meningitis
Cultures of CSF
take 4–8 weeks
233
In the evaluation of subacute meningitis, if spinal fluid examined by LP on two separate occasions fails to yield an organism, CSF should be obtained by
high-cervical or cisternal puncture
234
A highly sensitive and specific test for cryptococcal meningitis
Cryptococcal polysaccharide antigen test
Reactive test establishes the diagnosis
235
Specificity of 100% and a sensitivity of 75% for coccidioidal meningitis
CSF complement fixation antibody test
236
Treatment of TB meningitis with dose and duration
* Isoniazid (300 mg/d)
* Rifampin (10 mg/kg per day)
* Pyrazinamide (30 mg/kg per day in divided doses), iscontinued after 8 weeks
* Ethambutol (15–25 mg/kg per day in divided doses), may be discontinued once isolate antimicrobial sensitivity is known
6 month course
237
Dexamethasone dose in TB meningitis
12–16 mg/d for 3 weeks then tapered over 3 weeks
238
Treatment of meningitis due to C. neoformans in non-HIV, nontransplant patients
Induction therapy: Amphotericin B (AmB) (0.7 mg/kg IV per day) plus flucytosine (100 mg/kg per day in four divided doses) for at least 4 weeks if CSF culture results are negative after 2 weeks of treatment; Extended to 6 weeks if with neurologic complications
Consolidation therapy: Fluconazole 400 mg/d for 8 weeks
239
Treatment of meningitis due to C. neoformans in transplant recipients:
Liposomal AmB (3–4 mg/kg per day) or AmB lipid complex (ABLC) 5 mg/kg per day plus flucytosine (100 mg/kg per day in four divided doses) for at least 2 weeks or until CSF culture is sterile
Followed by an 8- to 10-week course of fluconazole (400–800 mg/d [6–12 mg/kg] PO). If the CSF culture is sterile after 10 weeks of acute therapy, the dose is decreased to 200 mg/d for 6 months to a year
240
Treatment of meningitis due to C. neoformans in HIV patients:
AmB or a lipid formulation plus flucytosine for at least 2 weeks
Followed by fluconazole for a minimum of 8 weeks
May require indefinite maintenance therapy with fluconazole 200 mg/d
241
Treatment of meningitis due to H. capsulatum:
AmB (0.7–1.0 mg/kg per day) for 4–12 weeks; total dose of 30 mg/kg is recommended; not discontinued until fungal cultures are sterile
Maintenance therapy: itraconazole 200 mg two or three times daily for at least 9 months to a year
242
Treatment of meningitis due to C. immitis:
High-dose fluconazole (1000 mg daily) as monotherapy
IV AmB (0.5–0.7 mg/kg per day) for >4 weeks
Lifelong therapy with fluconazole (200–400 mg daily) to prevent relapse
243
Most common complication of fungal meningitis
Hydrocephalus
244
Treatment of meningitis secondary to syphilis
Aqueous penicillin G in a dose of 3–4 million units intravenously every 4 h for 10–14 days
Alternative regimen: 2.4 million units of procaine penicillin G IM daily with 500 mg of oral probenecid four times daily for 10–14 days
Followed with 2.4 million units of benzathine penicillin G IM once a week for 3 weeks
245
In meningitis secondary to syphilis, CSF should be reexamined at
6-month intervals for 2 years
246
Empiric therapy of acute meningitis in immunocompetent children >3 months and adults <55
Cefotaxime, ceftriaxone, or cefepime + vancomycin
247
Empiric therapy of acute meningitis in adults >55 and adults of any age with alcoholism or other debilitating illnesses
Ampicillin + cefotaxime, ceftriaxone or cefepime + vancomycin
248
Empiric therapy of acute meningitis in hospital-acquired meningitis, posttraumatic or postneurosurgery meningitis, neutropenic patients, or patients with impaired cell- mediated immunity
Ampicillin + ceftazidime or meropenem + vancomycin
249
Glucocorticoid therapy for mild, moderate and severe MG
Mild or moderate weakness – 15-25 mg/d
Severe – high dose. Patients are maintained on the dose that seems to control their weakness for about a month, and then slowly tapered. Tapering is no faster than 10 mg a month until 20 mg daily and then 2.5-5 mg a month
250
Chronic meningitis neurologic syndrome exists for how long?
>4 week
251
Five most common causes of chronic meningitis:
1. Meningeal infections
2. Malignancy
3. Autoimmune inflammatory disorders
4. Chemical meningitis
5. Parameningeal infections
252
Cardinal features of chronic meningitis (may occur alone or in combination)(6)
1. Persistent headache
2. Hydrocephalus
3. Cranial neuropathies
4. Radiculopathies
5. Cognitive changes
6. Personality changes
253
Cerebrospinal fluid is produced by the ______ of the cerebral ventricles, then exits through narrow foramina into the _____ surrounding the brain and spinal cord, circulates around the _______ and over the _______, then resorbed by ______ projecting into the _____
```
Choroid plexus
subarachnoid space
base of the brain
cerebral hemispheres
superior sagittal sinus
```
Pathway provides rapid spread of infectious and other infiltrative processes over the brain, spinal cord, cranial, and spinal nerve roots
254
Arachnoid cuffs that surround the blood vessels that penetrate the brain tissue and may be a pathway of spread from the subarachnoid space into the brain parenchyma
Virchow-Robin spaces
255
Thickening of the meninges caused by clumping of the lower nerve roots due to chronic inflammation
Pachymeningitis
256
Major concern of chronic meningitis in the immunosuppressed patient (e.g. HIV patients)
chronic meningitis may present without headache or fever
257
Two clinical forms of chronic meningitis
1. Chronic and persistent symptoms
| 2. Recurrent, discrete episodes of illness
258
Recurrent meningitis that is most often due to herpes simplex virus (HSV) type 2
Mollaret’s meningitis
259
Recurrent meningitis that is due to episodic leakage from an epidermoid tumor, craniopharyngioma, or cholesteatoma into CSF
Chemical meningitis
260
Meningitis wherein fatal levels of raised ICP can occur without enlarged ventricles
Cryptococcal meningitis
261
This cells usually predominate in the CSF in most categories of chronic (not recurrent) meningitis
Mononuclear cells
262
Nonencapsulated brain abscess
Cerebritis
263
In up to 25% of cases of brain abscess, no obvious primary source of infection is apparent
cryptogenic brain abscess
264
Otogenic abscesses occur predominantly in the(2)
temporal lobe (55–75%) and cerebellum (20–30%)
265
In some series, up to 90% of cerebellar abscesses are
Otogenic
266
Abscesses that develop as a result of direct spread of infection from the frontal, ethmoidal, or sphenoidal sinuses and those that occur due to dental infections are usually located in the
frontal lobes
267
Hematogenous brain abscesses show a predilection for the
territory of the middle cerebral artery (i.e., posterior frontal or parietal lobes)
268
T or F. for bacterial invasion of brain parenchyma to occur, there must be preexisting or concomitant areas of ischemia, necrosis, or hypoxemia in brain tissue
True. The intact brain parenchyma is relatively resistant to infection
269
Stage of cerebritis that is characterized by a perivascular infiltration of inflammatory cells, which surround a central core of coagulative necrosis
early cerebritis stage (days 1–3)
270
Cerebritis stage characterized by pus formation that leads to enlargement of the necrotic center, which is surrounded at its border by an inflammatory infiltrate of macrophages and fibroblasts.
late cerebritis stage (days 4–9)
A thin capsule of fibroblasts and reticular fibers gradually develops, and the surrounding area of cerebral edema becomes more distinct than in the previous stage
271
Cerebritis stage characterized by the formation of a capsule that is better developed on the cortical than on the ventricular side of the lesion
third stage, early capsule formation (days 10–13)
272
This stage of cerebritis correlates with the appearance of a ring-enhancing capsule on neuroimaging studies
third stage, early capsule formation (days 10–13)
273
Cerebritis stage defined by a well-formed necrotic center surrounded by a dense collagenous capsule
final stage, late capsule formation (day 14 and beyond)
The surrounding area of cerebral edema has regressed, but marked gliosis with large numbers of reactive astrocytes has developed outside the capsule. This gliotic process may contribute to the development of seizures as a sequela of brain abscess
274
The classic clinical triad of brain abscess
headache, fever, and a focal neurologic deficit
present in <50% of cases
275
The most common symptom in patients with a brain abscess is
Headache
occurring in >75% of patients
constant, dull, aching sensation, either hemicranial or generalized, and it becomes progressively more severe and refractory to therapy
276
T or F. Fever is present in all patients of brain abscess.
False.
277
the most common localizing sign of a frontal lobe abscess
Hemiparesis
278
the most common localizing sign of a temporal lobe abscess
disturbance of language (dysphasia) or an upper homonymous quadrantanopia
279
the most common localizing sign of a cerebellar abscess
Nystagmus and ataxia
280
Imaging of choice for brain abscess
MRI
Better than CT for demonstrating abscesses in the early (cerebritis) stages and is superior to CT for identifying abscesses in the posterior fossa
281
T or F. LP should be performed in patients with suspected focal intracranial infections such as abscess or empyema.
False. CSF analysis contributes nothing to diagnosis or therapy, and LP increases the risk of herniation
282
Blood cultures are positive in ~10% of brain abscess cases overall but may be positive in >85% of patients with abscesses due to
Listeria
283
Empirical therapy of community-acquired brain abscess in an immunocompetent patient
third- or fourth-generation cephalosporin (e.g., cefotaxime, ceftriaxone, or cefepime) and metronidazole
284
In brain abscess patients with penetrating head trauma or recent neurosurgical procedures, treatment should include
ceftazidime and vancomycin
Meropenem plus vancomycin also provides good coverage in this setting
285
Medical therapy alone is not optimal for treatment of brain abscess and should be reserved for patients whose abscesses are: (4)
1. neurosurgically inaccessible
2. small (<2–3 cm)
3. nonencapsulated abscesses (cerebritis)
4. For patients whose condition is too tenuous to allow performance of a neurosurgical procedure
286
T or F. Brain abscess patients should receive prophylactic anticonvulsant therapy because of the high risk (~35%) of focal or generalized seizures
True. Anticonvulsant therapy is continued for at least 3 months after resolution of the abscess, and decisions regarding withdrawal are then based on the EEG
287
When do you give glucocorticoids in patients with brain abscess and what dose?
IV dexamethasone therapy 10 mg every 6
For patients with substantial periabscess edema and associated mass effect and increased ICP
Dexamethasone should be tapered as rapidly as possible to avoid delaying the natural process of encapsulation of the abscess
288
The most common parasitic disease of the CNS worldwide
Neurocysticercosis
289
Cause of neurocysticercosis
T. solium
290
The most common manifestation of neurocysticercosis
new-onset partial seizures with or without secondary generalization
291
Part of the T. solium that can often be visualized on MRI
Scolex
292
most common finding and evidence that the neurocysticercosis parasite is no longer viable
Parenchymal brain calcifications
293
Treatment of neurocysticercosis (3)
Albendazole 15 mg/kg per day in two doses for 8 days or praziquantel 50 mg/kg per day for 15 days
Prednisone or dexamethasone
Only cysts in the vesicular stage, where the cyst contains living larva (scolex seen on CT or MRI), and cysts in the colloidal stage as the larva degnerates (edema surrounds the lesion), are treated with anticysticidal therapy
There is universal agreement that calcified lesions do not need to be treated with anticysticidal therapy
294
Treatment of CNS toxoplasmosis
combination of sulfadiazine, 1.5–2.0 g orally qid, plus pyrimethamine, 100 mg orally to load, then 75–100 mg orally qd, plus folinic acid, 10–15 mg orally qd
Folinic acid is added to the regimen to prevent megaloblastic anemia
Therapy is continued until there is no evidence of active disease on neuroimaging studies, which typically takes at least 6 weeks, and then the dose of sulfadiazine is reduced to 2–4 g/d and pyrimethamine to 50 mg/d
Alternative: Clindamycin plus pyrimethamine
295
A collection of pus between the dura and arachnoid membranes
subdural empyema
296
The most common predisposing condition of subdural empyema
Sinusitis and typically involves the frontal sinuses
297
Sinusitis-associated subdral empyema has a striking predilection for
young males
possibly reflecting sex-related differences in sinus anatomy and development
298
The most common causative organisms of sinusitis-associated SDE
Aerobic and anaerobic streptococci, staphylococci, Enterobacteriaceae, and anaerobic bacteria
299
The most common causative organisms of SDE secondary to neurosurgical procedures
Staphylococci and gram-negative bacilli
300
SDE is often associated with other intracranial infections such as (3)
1. epidural empyema (40%)
2. Cortical thrombophlebitis (35%)
3. Intracranial abscess or cerebritis (>25%)
301
This condition should always be suspected in a patient with known sinusitis who presents with new CNS signs or symptoms
Subdural empyema
302
The most common complaint at the time of presentation of subdural empyema
Headache
303
The most common focal neurologic deficit of SDE
Contralateral hemiparesis or hemiplegia
Can occur from the direct effects of the SDE on the cortex or as a consequence of venous infa
304
The definitive step in the management of this SDE
Emergent neurosurgical evacuation of the empyema, either through craniotomy, craniectomy, or burr-hole drainage
305
Empirical antimicrobial therapy for community-acquired SDE should include a combination of
third-generation cephalosporin (e.g., cefotaxime or ceftriaxone), vancomycin, and metronidazole for a minimum of 3–4 weeks after SDE drainage
same with epidural abscess. Ceftazidime or meropenem should be substituted for ceftriaxone or cefotaxime in neurosurgical patients
306
A suppurative infection occurring in the potential space between the inner skull table and dura
Cranial epidural abscess
307
This CNS suppurative infection may develop contiguous to an area of osteomyelitis, when craniotomy is complicated by infection of the wound or bone flap
Epidural abscess
308
T or F. Cranial epidural abscesses may result from hematogenous spread of infection from extracranial primary sites
False
309
Usual causative organism of an epidural abscess that develops as a complication of craniotomy or compound skull fracture
Staphylococci or gram-negative organisms
310
Periorbital edema and Pott’s puffy tumor may be present in this CNS suppurative infection
Epidural abscess
Reflecting underlying associated frontal bone osteomyelitis
Present in ~40%
311
The diagnosis should be considered when fever and headache follow recent head trauma or occur in the setting of frontal sinusitis, mastoiditis, or otitis media
Epidural abscess
Other CNS suppurative infections may also be considered
312
Procedure of choice to demonstrate a cranial epidural abscess
Cranial MRI with gadolinium enhancement
313
septic venous thrombosis of cortical veins and sinuses that may occur as a complication of bacterial meningitis; SDE; epidural abscess; or infection in the skin of the face, paranasal sinuses, middle ear, or mastoid
Suppurative intracranial thrombophlebitis
314
largest of the venous sinuses
superior sagittal sinus
It receives blood from the frontal, parietal, and occipital superior cerebral veins and the diploic veins, which communicate with the meningeal veins
315
the most common sites of primary infection resulting in septic cavernous sinus thrombosis (2)
sphenoid and ethmoid sinuses
316
A transverse sinus thrombosis may also present with otitis media, sixth nerve palsy, and retroorbital or facial pain, a syndrome called
Gradenigo’s syndrome
317
T or F. The presence of a small intracerebral hemorrhage from septic thrombophlebitis is an absolute contraindication to heparin therapy
False. Not an absolute contraindication
318
Recent clinical trials have shown that systolic blood pressure (SBP) can be safely lowered acutely and rapidly to _____ in patients with spontaneous ICH whose initial SBP was 150–220 mmHg
<140 mmHg
319
a large phase 3 clinical trial to address the effect of acute blood pressure lowering on ICH functional outcome that revealed that there was a significant shift to improved outcomes in the lower blood pressure arm, whereas both groups had a similar mortality
INTERACT2 trial
INTERACT2 randomized patients with spontaneous ICH within 6 h of onset and a baseline SBP of 150–220 mmHg to two different SBP targets (<140 and <180 mmHg). In those with the target SBP <140 mmHg, 52% had an outcome of death or major disability at 90 days compared with 55.6% of those with a target SBP <180 mmHg (p = .06).
320
clinical trial to address the effect of acute blood pressure lowering on ICH functional outcome that demonstrated no difference in outcome between low and high BP
ATACH2
321
In patient with intracerebral hemorrhage, the recommended CPP that should be maintained is
50–70 mmHg
322
CPP is calculated by
MAP – ICP
323
ICH accounts for ____ of all strokes, and about _____ of patients die within the first month
~10%
35–45%
324
Most common causes of ICH (4)
1. Hypertension
2. Coagulopathy
3. Sympathomimetic drugs (cocaine, methamphetamine)
4. Cerebral amyloid angiopathy (CAA)
325
Hypertensive ICH usually results from spontaneous rupture of a ______ deep in the brain
small penetrating artery
326
Most common sites of hypertensive ICH (4)
1. basal ganglia (especially the putamen)
2. thalamus
3. cerebellum
4. pons
327
Most hypertensive ICHs initially develop over_____, whereas those associated with anticoagulant therapy may evolve for as long as _____
30–90 min
24–48 h
However, it is now recognized that about a third of patients even with no coagulopathy may have significant hematoma expansion with the first day
328
Within____, macrophages begin to phagocytize the blood in ICH at its outer surface
48 h
329
After_______, the ICH is generally resolved to a slitlike cavity lined with a glial scar and hemosiderin-laden macrophages
1–6 months
330
most common site for hypertensive hemorrhage
Putamen
adjacent internal capsule is usually damaged
331
Sentinel sign of hypertensive ICH
Contralateral hemiparesis
332
A prominent sensory deficit involving all modalities is usually present in this hypertensive ICH
Thalamic hemorrhages
Aphasia, often with preserved verbal repetition, may occur after hemorrhage into the dominant thalamus, and constructional apraxia or mutism occurs in some cases of nondominant hemorrhage
333
Thalamic hemorrhages cause several typical ocular disturbances by extension inferiorly into the
upper midbrain
deviation of the eyes downward and inward so that they appear to be looking at the nose, unequal pupils with absence of light reaction, skew deviation with the eye opposite the hemorrhage displaced downward and medially, ipsilateral Horner’s syndrome, absence of convergence, paralysis of vertical gaze, and retraction nystagmus
334
chronic, contralateral pain syndrome that occur later in thalamic hemorrhages
Déjérine-Roussy syndrome
335
deep coma with quadriplegia often occurs over a few minutes in this hypertensive ICH
pontine hemorrhages
prominent decerebrate rigidity and “pinpoint” (1 mm) pupils that react to light
336
impairment of reflex horizontal eye movements evoked by head turning (doll’s-head or oculocephalic maneuver) or by irrigation of the ears with ice water is usually seen in what hypertensive ICH
pontine hemorrhages
337
Most patients with deep coma from pontine hemorrhage ultimately die, or develop a______ , but small hemorrhages are compatible with survival and significant recovery
locked-in state
338
Hypertensive ICH that develop over several hours and are characterized by occipital headache, repeated vomiting, and ataxia of gait
Cerebellar hemorrhages
In mild cases, there may be no other neurologic signs except for gait ataxia. Dizziness or vertigo may be prominent
There is often paresis of conjugate lateral gaze toward the side of the hemorrhage, forced deviation of the eyes to the opposite side, or an ipsilateral sixth nerve palsy
339
The major neurologic deficit with an occipital hemorrhage
hemianopsia
340
The major neurologic deficit with a left temporal hemorrhage
aphasia and delirium
341
The major neurologic deficit with a parietal hemorrhage
hemisensory loss
342
The major neurologic deficit with a frontal hemorrhage
arm weakness
343
A disease of the elderly in which arteriolar degeneration occurs and amyloid is deposited in the walls of the cerebral arteries
Cerebral amyloid angiopathy
It accounts for some intracranial hemorrhages associated with IV thrombolysis given for myocardial infarction
344
the most common cause of lobar hemorrhage in the elderly
Cerebral amyloid angiopathy
345
This disorder can be suspected in patients who present with multiple hemorrhages (and infarcts) over several months or years or in patients with “microbleeds” in the cortex, seen on brain MRI sequences sensitive for hemosiderin (iron-sensitive imaging)
Cerebral amyloid angiopathy
346
definitively diagnosed by pathologic demonstration of Congo red staining of amyloid in cerebral vessels
Cerebral amyloid angiopathy
347
associated with increased risk of recurrent lobar hemorrhage and may therefore be markers of amyloid angiopathy
ε2 and ε4 allelic variations of the apolipoprotein E gene
348
Definitive diagnostic test for CAA
Cerebral biopsy
349
Drugs that are frequent causes of stroke in young (age <45 years) patients (2)
Cocaine and methamphetamine
The mechanism of sympathomimetic-related stroke is not known, but cocaine enhances sympathetic activity causing acute, sometimes severe, hypertension, and this may lead to hemorrhage
350
The common sites of ICH secondary to head injury (5)
```
Temporal lobe
Inferior frontal lobe
Subarachnoid
Subdural
Epidural spaces
```
351
Anticoagulant-related ICHs may occur at any location, but they are often
lobar or subdural
ICH associated with hematologic disorders (leukemia, aplastic anemia, thrombocytopenic purpura) can occur at any site and may present as multiple ICHs
352
Most common metastatic tumors associated with ICH (4)
Choriocarcinoma
Malignant melanoma
Renal cell carcinoma
Bronchogenic carcinoma
353
_______ in adults and ______ in children may have areas of ICH associated with the neoplasm
Glioblastoma multiforme
Medulloblastoma
354
Complication of malignant hypertension that present as headache, nausea, vomiting, convulsions, confusion, stupor, and coma
Hypertensive encephalopathy
There are retinal hemorrhages, exudates, papilledema (hypertensive retinopathy), and evidence of renal and cardiac disease
355
MRI brain imaging of hypertensive encephalopathy shows a pattern of typically (posterior/anterior?) edema that is (reversible or irreversible?) and termed ______
posterior (occipital > frontal) brain
reversible
reversible posterior leukoencephalopathy
356
Distinguishing hypertensive encephalopathy with ICH from hypertensive ICH is important since aggressive lowering of SBP to 140–180 mmHg acutely is usually considered in ____ but less aggressive measures should be used in _____
hypertensive ICH
hypertensive encephalopathy
Having no alteration in mental status or other prodrome prior to the ICH favors hypertensive ICH as the disease
357
Hemorrhages into the spinal cord are usually the result of (3)
AVM
Cavernous malformation
Metastatic tumor
358
A validated clinical grading scale that is useful for stratification of mortality risk and clinical outcome of ICH
ICH Score
359
A monoclonal antibody to dabigatran and the administration of two doses reverses the anticoagulation effect of dabigatran quickly
Idarucizumab
360
T or F. You may do platelet transfusion of ICH without thrombocytopenia but with intake of antiplatelet drugs
False. A recent clinical trial of platelet transfusions in patients with ICH and without thrombocytopenia who are taking antiplatelet drugs suggested no benefit and possible harm.
361
Trial that randomized patients with supratentorial ICH to either early surgical evacuation or initial medical management and no benefit was found in the early surgery arm
International Surgical Trial in Intracerebral Haemorrhage (STICH)
although analysis was complicated by the fact that 26% of patients in the initial medical management group ultimately had surgery for neurologic deterioration
362
Trial that revealed that surgery within 24 h of lobar, supratentorial hemorrhage did not improve overall outcome, but might have a role in select severely affected patients
STICH-II
Therefore, existing data do not support routine surgical evacuation of supratentorial hemorrhages in stable patients. However, many centers still consider surgery for patients deemed salvageable and who are experiencing progressive neurologic deterioration due to herniation
363
most cerebellar hematomas ____ in diameter will require surgical evacuation
>3 cm
Patients with hematomas between 1 and 3 cm require careful observation for signs of impaired consciousness, progressive hydrocephalus, and precipitous respiratory failure
If the patient is alert without focal brainstem signs and if the hematoma is <1 cm in diameter, surgical removal is usually unnecessary
364
T or F. Hyperventilation is one of the management of increased ICP in ICH
True, but limited to acute rescucitation only.
hyperventilation may actually produce ischemia by cerebral vasoconstriction
365
T or F. Glucocorticoids are helpful for the edema from intracerebral hematoma
False
366
congenital shunts between the arterial and venous systems that may present with headache, seizures, and intracranial hemorrhage
True AVMs
367
AVMs occur in all parts of the cerebral hemispheres, brainstem, and spinal cord, but the largest ones are most frequently located in the _____, commonly forming a wedge-shaped lesion extending from the cortex to the ventricle.
posterior half of the hemispheres
368
Familial AVM may be a part of the autosomal dominant syndrome of hereditary hemorrhagic telangiectasia syndrome called ______, which is due to mutations in either endoglin or activin receptor-like kinase 1, both involved in transforming growth factor (TGF) signaling and angiogenesis
Osler-Rendu-Weber syndrome
369
Most common involvement of ICH secondary to AVM
intraparenchymal
with extension into the subarachnoid space in some cases
370
Unlike primary subarachnoid hemorrhages, blood from a ruptured AVM is usually not deposited in the basal cisterns, and _______ is rare
symptomatic cerebral vasospasm
371
The risk of AVM rupture is strongly influenced by a
history of prior rupture
372
The AVM may be large enough to steal blood away from adjacent normal brain tissue or to increase venous pressure significantly to produce venous ischemia locally and in remote areas of the brain. This is seen most often with large AVMs in the
territory of the middle cerebral artery.
373
Large AVMs of the ______ may be associated with a systolic and diastolic bruit (sometimes self-audible) over the eye, forehead, or neck and a bounding carotid pulse
anterior circulation
374
Initial imaging of choice for cerebral AVM
MRI
although noncontrast CT scanning sometimes detects calcification of the AVM and contrast may demonstrate the abnormal blood vessels
375
gold standard for evaluating the precise anatomy of the cerebral AVM
conventional x-ray angiography
376
T or F. Venous anomalies in the brain are of little clinical significance and should be ignored if found incidentally on brain imaging studies
True
Surgical resection of these anomalies may result in venous infarction and hemorrhage. Venous anomalies may be associated with cavernous malformations (see below), which do carry some bleeding risk.
377
true capillary malformations that often form extensive vascular networks through an otherwise normal brain structure
Capillary telangiectasias
378
Typical locations of capillary telangiectasias (2)
pons and deep cerebral white matter
these capillary malformations can be seen in patients with hereditary hemorrhagic telangiectasia (Osler-Rendu-Weber) syndrome
379
tufts of capillary sinusoids that form within the deep hemispheric white matter and brainstem with no normal intervening neural structures
Cavernous angiomas
The pathogenesis is unclear. Familial cav- ernous angiomas have been mapped to several different genes: KRIT1, CCM2, and PDCD10
380
acquired connections usually from a dural artery to a dural sinus
Dural arteriovenous fistulas
381
In this acquired brain vascular lesion, patients may complain of a pulse-synchronous cephalic bruit (“pulsatile tinnitus”) and headache
Dural arteriovenous fistulas
382
Clinical and imaging factor and their in ICH scoring (5)
1. Age
<80 years – o
≥ 80 years – 1
2. Hematoma volume
<30 cc – 0
≥ 30 cc – 1
3. Intraventricular hemorrhage present
No – 0
Yes – 1
4. Infratentorial origin of hemorrhage
No – 0
Yes – 1
5. GCS score
13-15 – 0
5-12 – 1
3-4 – 2
