Transcript CM * Neuro Exam Topics

Block 3, Exam 2, Lecture 14-25
Sorry it seems like a lot (200+ slides)
BUT 65 slides are title slides
1.
2.
3.
4.
5.
6.
7.
Risk factors for CNS tumors
Occipital lobe
Glioblastoma treatments
Acute seizure management
Recurrent glioma treatment
Cells of neural origin
Chiari malformation herniations
1. Risk factors for CNS tumors
***Incidence***
Slight predominance M > F
 Caucasian > blacks

http://www.medinfographics.com/
Pathogenesis
Sequential accumulation of genetic aberrations
 Deregulation of growth-factor signaling pathways
 Loss of chromosomes 1p and 19q
 Defects in PTEN, Rb, p53, cell-cycle pathways

***Risk Factors***
•
Exposure to ionizing radiation
• Family history
• Genetic syndromes – important for risk
• Neurofibromatosis
• Tuberous sclerosis
• von Hippel-Lindau
• Basal cell nevus syndrome
• Li Fraumeni syndrome (p53)
• Turcot’s syndrome
2. Occipital lobe
Occipital lobe
controls…VISION!!!!
3. Glioblastoma treatments
Glioblastoma Multiforme
Glioblastoma (GBM)
•
Most common primary brain tumor
• Medial survival <1 yr
• Incidence rising in elderly population
• Requires craniotomy for biopsy
• No role for surgical resection
• Tx = Radiation and temozolamide better than
radiation alone – median survival 1218months
***GBM Tx**
Randomized study of RT versus RT plus
temozolomide followed by 6 months of adjuvant
temozolomide in patients with newly diagnosed
GBM demonstrated a statistically significant
increase in median survival of 3 months in the
combination-treated group.
 The 2-year survival rate was 26.5% in the
combination group compared with only 10.4% in the
radiation-only group.
 The treatment is relatively safe and well tolerated

R Stupp et al. N Engl J Med. 2005;352:987-996.
4. Acute seizure management
***Emergency Management***

Seizures:
1. Stabilize the environment
2. Anticonvulsants –
Ativan for acute management
Dilantin, Keppra, etc…
3. Imaging – MRI w/ gadolinium
5. Recurrent glioma treatment
***Recurrent Gliomas***
•
Re-excision
• Radiation – if not previously done
 CANNOT RE-RADIATE THE SAME AREA
Chemotherapy – nitrosureas, carboplatin, etoposide,
irinotecan, combinations
• Novel therapies
•
Recurrent GBM Tx
Glioblastoma are highly vascularized cancers
with elevated expression levels of vascular
endothelial growth factor (VEGF).
 Bevacizumab, a humanized monoclonal
antibody that targets VEGF, has been shown to
improve patient outcomes in combination with
chemotherapy.

6. Cells of neural origin
Sanai N et al. N Engl J Med 2005;353:811-822
7. Chiari malformation herniations
Tonsillar (Chiari) Herniation (6)
•
•
•
•
Posterior fossa tumors compress
the cerebellum downward into the
foramen magnum
Also called Chiari Malformation
Neuro findings: posterior
headache, cough induced
syncope, vomiting, respiratory
changes
Lhermittes Sign: dysesthesias in
the arms and legs with bending
the neck forward.
1.
2.
3.
4.
5.
Stages of sleep
Mechanism for deep sleep
Psychosocial insomnia tx
Diff Dx of childhood sleep disorders
Diagnosing sleep apnea
1. Stages of sleep
4 stages: 1,2,3, and REM
•
Stage 1 = shallow
(“church sleep”)
• Stage 2 = deep; slow
wave
• Stage 3 = stage 3 sleep;
some dreams
• Stage 4 = back to shallow
sleep (easily aroused) /
dream
2. Mechanism for deep sleep
Delta Waves…Deep Sleep…Stage 3
sleep
•
Also known as slow waves
• SWS or Stage 3 sleep
• 0.5 to 2 Hz frequency peak to peak
• Tall at least 75 mV
• Decrease in percentage once reach middle age
especially in men.
The S Phase
Sleep Homeostasis
 The expression of sleep need is based on the
amount of prior wakefulness.
 The process of sleeping is the only way to
reduce the homeostatic drive.
 Sleep Debt influences the depth and duration
of sleep.

3. Psychosocial insomnia tx
Definition
Most common complaint 30% of adults
 Repeated difficulty with sleep initiation and
continuity that results in daytime impairment
 Acute Insomnia


Psychosocial Insomnia – excessive focus and anxiety
about sleeping, racing thoughts, heightened somatic
tension…basically the life of a medical student…
Paradoxical Insomnia – sleep state
misperception, not aware of the amount of
sleep, sleep better away from home
 Drug or substance abuse including caffeine

Treatment of Insomnia…sleep hygiene
•
•
•
•
•
Stimulus Control – re associate the bed with quick
sleep onset (have a routine before bedtime, )
Sleep Restriction – no day naps, bedtime/wakeup at
same time everyday
Muscle Relaxation
Behavioral Therapy – modify attitudes not conducive to
sleep
Use of hypnotics should only be done after the above
with the goal to increase daytime functioning by
improving quality and quantity of sleep
4. Diff Dx of childhood sleep disorders
Disorders of NREM - Parsomnias

Confusional Arousals
 Sudden awakening, disorientation, confusion.

Sleep Terrors
 18 months to 5 yrs of age, violent and adrenergic event,
associated with complete amnesia

Somnoambulism – sleep walking
 Begins in adolescence
Somniloquy
 Bruxism
 Enuresis

Other Childhood Sleep Disorders

Limit setting behavioral insomnia
 Child has difficulty initiating or maintaining sleep
 Child refuses or stalls at an appropriate bed time or
upon awakening
 The caregiver demonstrates inappropriate limit setting
 Typically spoiled rotten 2 yr old boys
The silver lining with having young kids…it’s just good practice for the sleep
deprivation of residency!
Other Childhood Sleep Disorders

Sleep onset association disorder
 Children require an unnecessary object to initiate or
return to sleep.
 Falling asleep is an extended process with special
conditions.
 15 – 30% incidence between 6 months and 3 yrs of
age. Remits by 4 yrs of age.
 Typically boys.
5. Diagnosing sleep apnea
Polysomnography
Overnight study in a sleep lab with a technologist in
attendance is the gold standard for diagnosis of
OSA
 Can be done during the day for 3rd shift workers
 Studies can be diagnostic, cpap titration or split
night studies (Dx and Tx)
 EEG, EOG, EMG, EKG, airflow, respiratory motion,
limb movement, microphone and saturations.

1.
2.
3.
4.
5.
Management of Guillain-Barre
Symptoms of normal pressure hydrocephalus
Defining movement disorders
Sx of Charcot M-T vs. DM neuropathy vs. MS
Define radiculopathy
1. Management of Guillain-Barre
Acute Inflammatory Demyelinating
Polyradiculoneuropathy (AIDP)

Also known as Guillain-Barré Syndrome
 An acute autoimmune demyelinating
polyneuropathy
○ Mortality is 3% to 5%
○ This is a medical/neurological emergency that must be
recognized early to prevent significant morbidity and
mortality
Guillain-Barré Syndrome

Clinical features
 Symptoms usually begin with distal paresthesias




followed by ascending muscle weakness
Can affect cranial nerves
Can lead to respiratory failure
Serious complications may arise due to autonomic
dysfunction
Eventual loss of muscle stretch reflexes
Guillain-Barré Syndrome

Antecedent Events
 Viral infection
 Bacterial infection
○ Campylobacter jejuni
 Stress
○ Pregnancy
○ Surgery
○ Immunizations
 Often idiopathic
Guillain-Barré Syndrome

Diagnosis
 Clinical history and physical
 Lumbar puncture
○ Elevated protein with no cells
 Electrodiagnostic studies (Nerve Conduction) will be
abnormal early in the disease
Guillain-Barré Syndrome

Treatment
 Supportive care
○ Usually requires monitoring in a critical care setting
○ DVT prophylaxis
○ Nutritional support
○ Monitor vital signs
○ Pain management
○ Physical, occupational, speech therapies
 IVIG or plasma exchange
 ***There is absolutely no role for steroids***
Guillain-Barré Syndrome

Prognosis
 The disease usually plateaus around three weeks
 80% of patients will recover within 6 months
 15% of patients will have residual deficits
2. Symptoms of normal pressure
hydrocephalus
Normal Pressure Hydrocephalus
83 y/o left-handed female with a one year history of
progressive gait problems. She relates that it feels
like her feet are sticking to the floor. She also
reports recent onset of urinary incontinence. Her
family members have also noticed some mild short
term memory loss over the past couple of months.
Normal Pressure Hydrocephalus

Cardinal Features
 Gait ataxia
 Urinary incontinence
 Cognitive decline
3. Defining movement disorders
Tremor

Rhythmic oscillation of agonist and antagonist
muscles
Physiologic Tremor

Seen in all individuals to some degree when the
arms are outstretched
Essential Tremor
Postural or kinetic tremor
 Commonly involves the head

Cerebellar Tremor
Most problematic with voluntary movements
Rest Tremor
Parkinsonian tremor (“pill rolling”)
 Most obvious when the limb is fully supported and
at rest

Dystonia

Sustained muscular spasm that can be focal or
generalized
Focal Dystonias

Limb Dystonia
 Writer’s cramp
 Intermittent spasms of the foot or hand
Focal Dystonias

Blepharospasm
 Involuntary spasms of the orbicularis oculi, resulting in
eye closure
 Usually very easy to treat with Botox
Focal Dystonias

Torticollis (cervical dystonia)
 Involuntary twisting, turning, and tilting of the neck,
often associated with pain and tremor
 The treatment of choice is Botox
Focal Dystonias

Oromandibular Dystonia
 Facial grimacing, at times isolated to jaw opening or
closing
 Meige’s Syndrome consists of eye and jaw movements
Focal Dystonias

Spasmodic Dysphonia
 Intermittent spasms of the vocal cords
Tics

Sudden, fast, irregular movements, usually repeated
in the same muscle group
 Motor: simple vs complicated
 Vocal: simple vs complicated
 Tourette’s syndrome: multiple motor tics with at least one
vocal tic
Chorea
Quick, irregular, often semi-purposeful movements
 Think…Huntington’s Dance

Hemiballismus
Hemi – one side of the body
 Ballismus – think belligerent…violent type of
flinging movements

Myoclonus…convulsion

Sudden, fast movements, usually repeated in the
same body part
 Can be treated with various anticonvulsants
○ Valproate
○ Lamotrigine
○ Levetriacetam
○ Clonazepam
Tardive Dyskinesia
Combined chorea and dystonic movements, usually
in the face or lower jaw, but may be generalized
 Commonly associated with exposure to neuroleptic
medications
 The best way to manage this condition is to prevent
it from occurring in the first place

4. Various symptoms: 1) Charcot M-T,
2) DM Neuropathy, 3) MS
Symptoms of Charcot M-T








Onset of symptoms usually in the first decade (but
can occur as late as the fifth decade)
Weakness and wasting of the lower limbs then
progresses to upper limbs (trunk and proximal
muscles are usually spared)
Greatly reduced sensation (vibration and
proprioception…PCML!)
Pes cavus deformities of the feet
Contractures of wrists and fingers as disease
progresses
Scoliosis
Motor nerve conduction velocities are slowed
Can be associated with sensorineural hearing loss
Symptoms of DM Neuropathy
Pain
 Parasthesias
 Loss of sensation
 Paresis
 Imbalance

Symptoms of MS (multiple sclerosis)
From Dr. Sarko’s lecture 5
 Monocular blindness (due to lesions of the optic
nerve)
 Double vision (lesions of the medial longitudinal
fasciculus)
 Motor weakness/paralysis (due to lesions of the
corticospinal tracts)
 Abnormal somatic sensations
 Dizziness (due to lesions of the vestibular
pathways)
5. Define radiculopathy
Definitions

Mononeuritis multiplex
 Abnormality of multiple nerves independently
involving different limbs simultaneously

Radiculopathy
 Abnormality at the nerve root

Polyradiculopathy
 Abnormalities involving multiple nerve root levels

Polyradiculoneuropathy
 Abnormalities involving multiple nerve roots and
nerve trunks
More Definitions (extra info)

Peripheral neuropathy
 A general term for dysfunction of the peripheral
nervous system

Neuronopathy
 Dysfunction of the nerve cell body

Polyneuropathy
 Dysfunction of multiple nerves

Mononeuropathy
 Dysfunction of a single nerve, usually due to
entrapment
1.
2.
3.
4.
5.
Signs of Parkinson’s
Define essential tremor
Wilson’s disease signs
Compare Tic, tremor, chorea, dystonia, hemiballimus
Huntington’s characteristics
1. Signs of Parkinson’s
Parkinson’s Disease
64 y/o right-handed male with a six-month history
of tremor of the right hand. For the past three
months he has noted some soreness in the right
shoulder. His wife reports that he has been walking
more slowly for the past few months as well.
Parkinson’s Disease
Cardinal Features
 Rest Tremor - Parkinsonian tremor (“pill rolling”)
 Most obvious when the limb is fully supported and at rest
Bradykinesia
 Rigidity
 Postural instability

2. Define essential tremor
Essential Tremor
Postural or kinetic tremor (think, it’s essential to get
moving…kinetic)
 Commonly involves the head

3. Wilson’s disease signs
Clinical features of Wilson’s Disease
Age at onset ranges from 5-50 years, peaking
between 8 and 16 years
 Neurological symptoms are present in 40% of
affected individuals at the onset

 Movement disorders (tremor, dystonia, rigidity,
bradykinesia, etc…)
 Dysarthria, particularly in adults
 Psychiatric symptoms
Clinical features of Wilson’s Disease


Liver dysfunction (cirrhosis,
chronic active hepatitis)
Deposition of copper in iris
seen on slit lamp examination
(Kayser-Fleischer rings)
4. Compare Tic, tremor, chorea,
dystonia, hemiballimus (repeat
slides…jump to slide 92 if you want)
Tics

Sudden, fast, irregular movements, usually repeated
in the same muscle group
 Motor: simple vs complicated
 Vocal: simple vs complicated
 Tourette’s syndrome: multiple motor tics with at least one
vocal tic
Tremor

Rhythmic oscillation of agonist and antagonist
muscles
Chorea
Quick, irregular, often semi-purposeful movements
 Think…Huntington’s Dance

Dystonia

Sustained muscular spasm that can be focal or
generalized
Focal Dystonias

Limb Dystonia
 Writer’s cramp
 Intermittent spasms of the foot or hand
Focal Dystonias

Blepharospasm
 Involuntary spasms of the orbicularis oculi, resulting in
eye closure
 Usually very easy to treat with Botox
Focal Dystonias

Torticollis (cervical dystonia)
 Involuntary twisting, turning, and tilting of the neck,
often associated with pain and tremor
 The treatment of choice is Botox
Focal Dystonias

Oromandibular Dystonia
 Facial grimacing, at times isolated to jaw opening or
closing
 Meige’s Syndrome consists of eye and jaw movements
Focal Dystonias

Spasmodic Dysphonia
 Intermittent spasms of the vocal cords
Hemiballismus
Hemi – one side of the body
 Ballismus – think belligerent…violent type of
flinging movements

5. Huntington’s characteristics
Clinical features of Huntington’s
Disease






Various movement problems, with chorea being the
most common motor manifestation
Bradykinesia coexists with chorea
Cognitive decline
Psychiatric abnormalities
An abnormality of saccadic eye movements may be the
first neurological signs
Typical onset is in the fourth or fifth decade, but 10%
may have symptoms before the age of 20 (juvenile
Huntington’s)
1.
2.
3.
4.
5.
6.
7.
Presentation of H flu meningitis 8.
Bird meningitis
9.
STD meningitis
Pig meningitis
Virulence factors for dissemination 10.
11.
KNOW Listeria, e-coli, strep
12.
pneumo, Neisseria micro!
HIV meningitis bug and imaging
13.
findings
Hydrophobia
Compare common viruses in
meningitis (symptoms, time of
year, history)
Treatment of viral meningitis
Diagnosing fungal meningitis
Meningitis treatment in
splenectomy pt
How to tx PCN allergic pt with
syphilis
1. Presentation of H flu meningitis
History (Meningitis in Children)
 Altered Cry (80%)
o
o
o
o
High-pitched
Inconsolable
Weak or Moaning
Absence
 Lethargy (drowsy, indifferent)
o 50% of bacterial cases; 40% of viral cases
 Vomiting
o Often follows onset of fever
 Neck Stiffness (nuchal rigidity)
o When try to move head back, child grimaces
 Seizures
o Often occur within first few days of illness
 Headache/Irritability
Haemophilus influenzae type b (Hib)
Microbiology
 Unencapsulated strains colonize ~75% of
healthy children and adults; a minority colonize
Hib
Pathogenesis
URT colonization
 Virulence
o Polyribitol phosphate (PRP) Capsule
•
•
•
•
Adherence
Blocks phagocytosis and complement activation
Inhibits ciliary action
Prognosis associated with anti-PRP response
o Fimbriae
o IgA protease
BACTEREMIA
REPLICATION
Patient lacks Ig (6mo-2/3y)
Lungs
2. Presentation of Bird meningitis
Cryptococcus neoformans
Microbiology
 Most common pathogen causing fungal
meningitis
 Primarily an opportunistic infection
 Virulence
Pathogenesis
Replicates in bird
feces & eucalyptus
trees
o Polysaccharide Capsule
•
•
Antiphagocytic
Immune dysfunction
 Capsule released in copious amounts
 Little to no inflammation as capsule
polysaccharide prevents adhesion of
immune cells to endothelia
o Melanin production
•
•
•
Melanins contain stable populations of freeradicals
Protect from host production of oxidants
(phagocytes)
Less susceptibility to amphotericin B
FUNGEMIA
Lungs
Latency?
Granuloma?
Normal flora?
Skin
Histoplasma capsulatum
Microbiology
Pathogenesis
 Most prevalent endemic mycoses in N. America
o Found in Ohio and Mississippi river valleys
Inhalation of
microconidia
 Soil enriched with bird or bat droppings
enriches growth of fungus
o Cases from spelunking, excavation, cleaning
chicken coops, demolition/remodeling of
buildings, cutting down dead trees
 Virulence
o Prevent acidification of phagolysosome in
macrophages
o Iron-acquisition enzymes
Histoplasma infects
macrophages and
converts into yeasts
(image to left)
Lungs
Lymphatics
N
Granulomas form in
lymph nodes, liver
and spleen
(prevents
dissemination)
Macrophage
Multiple Organs
Immune
deficiency
Granuloma
3. Presentation of STD meningitis
Treponema pallidum
Microbiology
3 stage disease:
Primary Syphilis
–
Painless papule (chancre)
– 4-6 wk duration
Secondary Syphilis
– Rash (macular, papular, pustule) and flu-like illness
(hepatitis, arthritis, meningitis,…occurs)
– Also present on palms of hands and soles of feet
– 2 wk duration
Latent Syphilis
Pathogenesis
Sexual
transmission
Treponema
penetrates mucus
membranes via
abrasions during
sex
• Lesion (gumma) development in multiple organs
• Occurs 1-20 y after secondary syphilis
• Asymptomatic Neurosyphilis (CSF
abnormal)
 Mononuclear pleocytosis
 Increased protein conc
• Symptomatic Neurosyphilis
 Meningitis <1y after infection
 Meningitis + cerebral vasculitis
 Widespread brain parenchymal
damage (delusions, hallucinations,
memory and speech loss, impaired
judgement, balance loss, trouble
walking, altered personality)
Primary
Syphilis
Lymphatics
Secondary Syphilis
MANY TISSUES
Asymptomatic Neurosyphilis
Symptomatic Neurosyphilis
Meningitis
(1-2% of
cases)
4. Presentation of Pig meningitis
Taenia solium (Pork Tapeworm)
Microbiology & Clinical Manifestations
 Normal infection follows 1-4 (see pathogenesis)
o Pigs (intermediate host) acquire infection by
eating egg/proglottid-contaminated foods
o Humans, in turn, eat cysticerci-infected
undercooked pork which then develop into
mature worms in the intestines
 Neurocysticercosis follows 5-7 (see pathogenesis)
o Humans inadvertently consume
eggs/proglottids (usually autoinfection) which
penetrate intestinal wall and develop into
cysticerci in tissues (CNS here)
 Neurocysticercosis is the most common parasitic
disease of CNS worldwide
o Seizures
o Hydrocephalus (from obstruction of CSF
flow)
o Headache
o Nausea and vomiting
 intracranial pressure
o Vision difficulties
o Dizziness and ataxia
o Altered mental status
o Chronic meningitis (cysticerci in
subarachnoid)
Pathogenesis
Toxoplasma gondii
Microbiology
 Nonfeline stage (human, intermediate host)
o Oocysts (cat feces) or bradyzoites
(undercooked pork, lamb, beef) ingested and
rapidly form tachyzoites
o Tachyzoites can infect/replicate in any cell
exc. RBC
o Tachyzoites replicate in parasitophorous
vacuole in host cells until rupture – adjacent
cells are then infected
o Primary sites of replication are CNS and
muscle
 Feline stage
o Cats consume infected animals (rodents)
harboring bradyzoites which then carry out the
sexual phase in the cat producing oocysts
 By adulthood, 50% of Americans are seropositive
for T. gondii
Pathogenesis
Toxoplasma gondii
Clinical Manifestations
 Immunocompetent Patients…healthy ppl
o
o
o
o
o
o
Cervical lymphadenopathy
Headache
Fever and Myalgia
Sore throat
Abdominal pain
Meningoencephalitis
•
•
•
Mononuclear pleocytosis
 intracranial pressure
 CSF protein conc.
 Immunosuppressed Patients…think HIV pt’s
Principle CNS infection of patients with AIDS
Altered mental status
Seizures
Headaches
Mass lesions (basal ganglia, brainstem,
pituitary)
o Focal lesions
o
o
o
o
o
•
•
•
•
•
Motor deficits
Cranial nerve palsies
Movement disorders
Visual field loss
Aphasia
Pathogenesis
5. Virulence factors for dissemination
Streptococcus pneumoniae
(Pneumococcus)
Pneumolysin

Cytotoxic to endothelial cells (dissemination)
Neisseria meningitidis
(Meningococcus)
Intracellular survival in PMN
 Allows
infection of inflamed tissue as
PMN migrate to those sites
Listeria monocytogenes
Listeriolysin O & Phospholipase B
 Induces uptake by epithelia and/or
phagocytes
 Enzymes activated in endosome/phagosome
 Escape into cytosol & replicate
ActA & Actin tails
 Propel bacteria into host cell membrane
and into adjacent cells
6. KNOW Listeria, e-coli, strep
pneumo, Neisseria micro!
Listeria

Common cause of bacterial meningitis in adults
(>50yo) & children (0-6 mos.
Listeria monocytogenes
Microbiology
Pathogenesis
Ingestion of
contaminated meat or
dairy
 Foodborne illness in adults (processed meat
and dairy products) and meningitis in
newborns
 High risk – pregnant women, neonates,
immunocompromised patients, elderly
 Virulence
o Listeriolysin O & Phospholipase B
• Induces uptake by epithelia
and/or phagocytes
• Enzymes activated in
endosome/phagosome
• Escape into cytosol & replicate
o ActA & Actin tails
• Propel bacteria into host cell
membrane and into adjacent cells
Spleen
CELLULAR
BACTEREMIA
Reduced
Th1 or
Th17
response
E. Coli
Common cause of bacterial meningitis in adults
( and children (0-6 mos.)
 Common cause of brain abscess in
immunocompromised individuals

Streptococcus pneumonia
Common cause of bacterial meningitis
 Common cause of brain abscess in
immunocompromised individuals

Streptococcus pneumoniae (Pneumococcus)
Microbiology
 Colonizes ~10% of healthy adults, ~40% of healthy
children (transient…6 wks–6 mo)
 Virulence
o Polysaccharide Capsule
• Blocks phagocytosis and complement
activation
o Pneumolysin
• Peroxides build up  induce autolysins
 pneumolysin released
• Cytotoxic to endothelial cells
(dissemination)
• Inhibits phagocytosis & adaptive
response
• Inhibits ciliary action
• Stimulates chemotaxis of PMN (to
promote inflammation)
o C-substance
• Attachment site for virulence factors
• Adherence to various human cells
o Pneumococcal surface protein A (PspA) &
Pneumococcal surface adhesin A (PsaA)
• Block phagocytosis
Pathogenesis
URT colonization
BACTEREMIA
REPLICATION
Lack of ability to clear
Lungs
CAMP Test
• The -lysin produced by -hemolytic Staphylococcus aureus acts synergistically with the CAMP
factor produced by both -hemolytic and nonhemolytic Streptococcus agalactiae (group B)
• This synergistic reaction results in an enhanced and very visible zone of hemolysis in the region
between the two cultures
• The synergistic zone is not observed in group A, C, and G Streptococcus
Neisseria
Common Causes of Bacterial Meningitis in
Children (6mos – 6 yo)
 Common Causes of Bacterial Meningitis in
Adults (military recruits and dorm residents)

Neisseria meningitidis (Meningococcus)
Microbiology
 Leading cause of bacterial meningitis in
children and young adults in US (cold, dry
months)
 Virulence
o Lipooligosaccharide (LOS)
• 10X more toxic than LPS
• Ag variation
• When sialyated  inhibits
complement deposition
• Temps above/below 37C  LOS
breakdown (autolysis)
o Polysaccharide Capsule
• Divide into serogroups (A-C, Y, W135)
o Intracellular survival in PMN
• Allows infection of inflamed tissue
as PMN migrate to those sites
o Fimbriae
• Attachment to non-ciliated epithelia
o Porins
• B cell mitogens
Pathogenesis
URT colonization
DIC
Shock
Petechia
Purpura
LOS
*
Rapid
replicatio
n
BACTEREMIA
Slow
replicatio
n
REPLICATION
*LOS loosely held to
peptidoglycan (easily shed)
Joints
7. HIV meningitis bug and imaging
findings
HIV stuff

Infectious Causes of Aseptic Meningitis
Agents of Subacute/Chronic Meningitis
 Presentation
o 42-year-old white male was brought to the ER because of 2 week history
of fever, severe headache, nausea, vomiting and changes in mental status
o The patient was previously diagnosed with
currently not taking antiretroviral therapy
 Physical
o
o
o
o
o
 Lab
HIV two years ago and is
101.5F
(98.6)
P = 106/min
(60-100)
BP = 110/62
(90-150/50-90)
Nuchal rigidity
Positive Kernig sign (flexing of neck when
knee is flexed)
o Blood
•
WBC = 3,100/l (4,000-11,000)
 70% PMN
(50-60%)
 12% Lymphocytes
o Head CT is normal
Brain Abscess
Microbiology
 ~0.3-1/100,000 persons each year
 Predisposing conditions:
o Otitis media and mastoiditis (~33% of cases), sinusitis (10%), feverish infections of chest,
penetrating head trauma, neurosurgery, dental infections (~2%)
Pathogenesis
 Must be preexisting areas of ischemia, necrosis or hypoxia in brain tissue
o Early stage (1-3 d)
•
Inflammatory cell infiltration – surround central core of necrosis
•
•
Pus forms enlarging necrotic center
Surrounded by macrophages and fibroblasts
•
Collagenous capsule initiates
o Late stage (4-9 d)
o Capsule formation (10-13 d)
o Late capsule formation (>14 d)
• Well-formed necrotic center and surrounding capsule
Diagnostic Work-Up
MRI and CT studies – increased signal/low
diffusion coefficient (as compared to brain tumors)
 Needle aspiration – Gram stain/culture
 Peripheral leukocytosis, elevated C-reactive protein and ESR (erythrocyte sedimentation rate)
8. Hydrophobia
Agents of Viral Encephalitis
Presentation
o31-year old white man brought to ER with fever and visual hallucinations.
o4 days before arrival, patient developed malaise and back pain while working on
roadside clean-up crew. He was treated for muscle pain, vomiting, and abdominal
cramps with acetaminiphen prior to ER visit.
Physical
o100.04F
(98.6)
oP = 116/min
(60-100)
oBP =168/104
(90-150/50-90)
oPatient alert, with increased tone in right forearm and hyperesthesia over entire right
side of body.
oWatched for 12 hours-he became increasingly agitated and less well oriented.
oDeveloped hydrophobia
oHypersalivation and wide fluctuations in body temperature and blood pressure
Lab
oBlood
•WBC = 6,600/l (4,000-11,000)
•Differential: Normal
•Blood gas: Normal
•Serum chemistries: Normal
oBrain CT and chest X-ray normal
Rhabdoviruses
Microbiology
Rabies has the highest case-fatality (~100%) rate of any infectious disease once
clinical symptoms are observed.
-RNA, enveloped virus
Begins with typical viral syndrome leading to acute encephalomyelitis
Most common clinical symptoms:
Hypersalivation
Hydrophobia
Aerophobia
Transmission typically by raccoons, but dogs, foxes, skunks, bats, squirrels can be
involved
Diagnosis in humans
Test are performed on samples of saliva-virus isolation, RT-PCR
Serum and spinal fluid can be tested for Abs
Skin biopsies of hair follicles at the nape of neck-rabies antigen in cutaneous
nerve at base of hair follicle
9. Compare common viruses in
meningitis (symptoms, time of year,
history)
CNS viruses
Non-Human
Vector
Seasonal
Diagnosis
Antiviral
Rx
Group
Examples
Onset
Vaccine
Enteroviruses
Coxsackie viruses
Echovirus
Poliovirus
Acute to
subacute
None
Yes
•Clinical
•CSF exam/PCR
•Culture
No
No
(except
polio)
Herpes virus
Herpes simplex
virus (HSV)
Herpes B virus
Acute
(Latency)
None
No
•Clinical
•CSF exam/PCR
•EEG/MRI
Yes
No
Arboviruses
West Nile virus
(WNV)
Eastern equine
encephalitis virus
(EEEV)
La Crosse virus
(LACV)
Acute
Insects
Yes
•Clinical (exposure)
•CSF exam/PCR or
serologist
No
No for
most
Rabies
-
Subacute
to chronic
Animals
No
•Clinical syndrome
including exposure
•Skin biopsy
•CSF/peripheral
serologies
•Postmortem exam
No
Yes
Clinical Manifestations of Viral Meningitis

Signs and Symptoms:
 May be preceded by nonspecific viral syndrome
 Fever
 Headache
 stiff/ neck/nuchal rigidity
 Malaise
 Nausea
 Vomiting
 Chills
Review of Diagnostic Results for
Aseptic Meningitis
Typical CSF findings include elevated leukocyte
count (10-1000 mononuclear cells)
 Typically normal glucose
 Usually slightly elevated protein
 Other test include acute and convalescent viral
antibody titers and PCR for viral nucleic acid

Specific Viral Causes of Aseptic
Meningitis

Enterovirus- >85% of viral meningitis cases
 Coxsackieviruses
 Echovirus

Herpes simplex virus 2
Common Causes of Viral Meningitis
in Teenagers
Arbovirus
 Enteroviruses
 Herpes Simplex Virus 2

Echovirus
Microbiology
Echovirus=Enteric Cytopathic Human Orphan
viruses
Over 30 serotypes
First identified by cell culture from faeces of
patients suffering from paralytic and nonparalytic
illness.
Infection common in
summer and fall
Symptoms occur after a short incubation period
of 3-5 days.
Can have epidemic potential
Echo-V highly infectious and preferentially target
infants and young children
Coxsackie virus A and B
Microbiology
Coxsackievirus meningitis is seen most
frequently in children<5
Infants highly susceptible meningitis
and encephalitis
Aseptic meningitis is a common
manifestation due to Group B viruses.
Hand, Foot and Mouth Disease is a Group
A virus.
Typically, symptoms last a week.
Most cases seen in the summer.
Bind to CAR or DAF on cells surface
10. Treatment of viral meningitis
Rabies Treatments (encephalitis…)

General measures
 Cleaning of wound

Anti-rabies prophylaxis
 Passive administration of
Human rabies immunoglobulin
(HRIG)
 Human diploid cell vaccine
(HDCV)
CNS viruses
Non-Human
Vector
Seasonal
Diagnosis
Antiviral
Rx
Group
Examples
Onset
Vaccine
Enteroviruses
Coxsackie viruses
Echovirus
Poliovirus
Acute to
subacute
None
Yes
•Clinical
•CSF exam/PCR
•Culture
No
No
(except
polio)
Herpes virus
Herpes simplex
virus (HSV)
Herpes B virus
Acute
(Latency)
None
No
•Clinical
•CSF exam/PCR
•EEG/MRI
Yes
No
Arboviruses
West Nile virus
(WNV)
Eastern equine
encephalitis virus
(EEEV)
La Crosse virus
(LACV)
Acute
Insects
Yes
•Clinical (exposure)
•CSF exam/PCR or
serologist
No
No for
most
Rabies
-
Subacute
to chronic
Animals
No
•Clinical syndrome
including exposure
•Skin biopsy
•CSF/peripheral
serologies
•Postmortem exam
No
Yes
11. Diagnosing fungal meningitis
Characteristics of the CSF in
different types of meningitis
Type of
meningitis
Leukocytes
/mm3
(range)
Predominant cell
type
Glucose
Protein
Microbiological
Tests
Bacterial
0-60,000
Neutrophils
Very low (<520 mg/dL)
Elevated
Positive
Tuberculosis
25-500
Mononuclear cells
Low (20-40
mg/dL)
Elevated
Negative
Viral
0-1,000
Mononuclear cells
Normal (65-70
mg/dL)
Normal to
slightly
elevated
Negative
Fungal
0-1,000
Mononuclear
cells
Low (20-40
mg/dL)
Elevated
Negative
Dx of fungal meningitis


Slide 9 (notes) - Low glucose levels and a lymphocytic
pleocytosis (low WBC) should suggest the presence
of fungal, listerial, or tuberculosis meningitis.
Slide 10 (notes) - For fungus,




India ink tests,
Fungal cultures,
Agglutination tests for fungal antigens may be positive.
Slide 36 –


LP (CSF exam/culture)
PCR
Mycobacterium tuberculosis
Diagnostic Work-Up – Tuberculosis
Meningitis
 Night sweats
 Lumbar puncture
oCSF exam
• Acid-fast bacillus
 Red coloration
 Stain of cell wall mycolic
acid
• Lymphocyte pleocytosis (10500 cells/l)
 Also possible in fungal
meningitis
oCSF culture
• Growth on Lowenstein-Jensen
Egg media
 4-8 wks
 Acid-fast bacillus
 PCR
o Mycobacterium DNA
Acid-fast stain
12. Meningitis treatment in
splenectomy pt
PROPHYLACTIC PCN
Five splenectomized patients suffered six episodes of bacterial
meningitis with positive cerebrospinal fluid cultures. They were
admitted to the Nottingham hospitals between 1974 and 1985.
The infecting organism in all cases was Streptococcus
pneumoniae. Only one patient, who survived, had had
pneumococcal vaccine; two patients died in spite of intensive
therapy. There is now good evidence for giving prophylactic
penicillin to asplenic patients but the efficacy of the
pneumococcal vaccine remains uncertain.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1292085/
13. How to tx PCN allergic pt with
syphilis
 Doxycycline
or TCN
 Who knows?
1.
2.
3.
4.
5.
Non-contrast CT most useful for
How does MRI work
Gadolinium contraindications
MRI least useful for
Know common imaging structures
***Take home points***
1. The precise details of structures in the brainstem/midbrain/spinal
cord are not well visualized on CT scans and better seen on MR.
2. CT does involve exposure to radiation.
3. MR can be time-consuming and patient has to hold still longer.
4. Both CT and MR are expensive examinations
5. In most cases, the first examination to perform is CT, but MRI remains
the “gold standard”.
EXAM QUESTIONS!!!
1. Non-contrast CT most useful for
what?
CVA workup
Non-contrast CT is most efficient method of
acute stroke (within 24hrs)
Goals for imaging:
1. To exclude other causes for neurological
symptoms such as brain tumor,
intraparenchymal or subarachnoid bleed.
2. Identify any hemorrhagic component
3. Determine whether there is evidence of acute
infarction, when it occurred and how extensive it
is.
2. How does MRI work
MRI
No radiation
 Electromagnetic field uses protons (free
hydrogen atoms) to obtain images
 Signal is received as the protons release their
energy
 Various sequences are used to optimize signal
intensity and pathology
 “Signal intensity” is used to describe images
high=bright, low=dark

MRI terminology
Field Strength - 1 Tesla = 10000 Gauss. Most
clinical MRI’s are 1.5T or 3.0T
 Radiofrequency (RF) coils are one of the most
important components that affect image quality.
 T1 relaxation - T1 is defined as the time it
takes for the longitudinal magnetization (Mz) to
reach 63 % of the original magnetization.
 T2 relaxation – T2 is defined as the time it
takes for the spins to de-phase to 37% of the
original value.

3. Gadolinium contraindications
MRI contrast
Gadolinium based – paramagnetic agent
causes T1 shortening (hyperintensity)
 Rare-earth heavy metal ion
 Used to accentuate pathology (similar to
iodinated contrast for CT)
 Contraindications: Allergy, pregnancy, lactation,
renal failure (nephrogenic systemic fibrosis)

4. MRI least useful for what?
MRI
NO RADIATION
 Tumors
 Acute stroke
 Cord injury
 INFECTION
 Soft tissue detail (ligaments,
cartilage)








Advantages
Expensive
Time – 30-45m
Safety
Not great for bone detail,
but good for marrow
abnormalities
Motion
Claustrophobia
Pacemaker
Disadvantages
5. Know common imaging structures
Common structures to Image
CNS vasculature (aa and vv)
 Brain (Cerebrum, ventricles, cerebellum)
 Midbrain, pons, medulla
 Spinal Cord


KNOW 4th ventricle and pons
***EXAM!!!***
Quadgrigeminal
Midbrain
(mesencephalon)
Pons
plate cistern
Cerebral
aqueduct
4th ventricle
Basilar
artery
Medulla
Cisterna
magna
***CT anatomy***
***CT anatomy***
1.
2.
3.
4.
5.
6.
7.
Best test to exclude meningitis
Extra axial brain neoplasms
Skull fractures and hemorrhage
Early imaging finding of infarction
Intramedullary spine lesions
Spinal cord met findings
MS MRI findings
1. Best test to exclude meningitis
R/o meningitis
In this order:
1. Clinical Workup = History & Physical
2. Imaging
3. Lumbar puncture (LP…aka CSF studies)

See reference slide (next slide)
***Meningitis***







Acute or chronic inflammatory infiltration of pia, arachnoid
and CSF
Classified as acute pyogenic (bacterial), lymphocytic (viral),
chronic (tuberculosis or granulomatous)
Hematogenous spread from remote infection is most common
etiology.
Direct extension from sinusitis, orbital cellulitis, mastoiditis,
otitis media is much less common
Diagnosis of bacterial meningitis is a clinical one (1ST)
and confirmed by CSF studies
Imaging (2nd) is important to exclude other
diagnosis/complications before spinal tap (3rd).
aka…Clinical Dx > imaging > spinal tap/CSF study
2. Extra axial brain neoplasms
Neoplasm
Questions to answer when working up a brain
mass/lesion:
1. Intra-axial (within the brain) vs. extra-axial
(outside the brain)?
2. Solid or multiple?
3. Gray matter or white matter;
4. Lesion distribution; Supra or infra-tentorial brain?
5. Enhancement characteristics
6. Signal intensity (MRI) or attenuation pattern (CT)
Neoplasm
NON-GLIAL = EXTRA-AXIAL
Meningioma
-Extra-axial mass with
broad-based dural
attachment
-Intense, homogeneous
enhacement
-Most common radiationinduced tumor, 20-35yr
latency
-<10% are sympotmatic (die
with and not of)
-Mostly isolated but
associated with NF2
3. Skull fractures and hemorrhage
Subdural Hematoma







Blood collection between dura
and arachnoid
Up to 30% of patients with
closed head injury
50-90% mortality rate
Younger patients – MVA
Older – Falls
Shearing of bridging veins
Crescentic, may cross sutures
Epidural Hematoma





Blood collection between
skull and dura
Does not cross sutures
Associated with skull fx
(>95%)
Lentiform configuration
Mostly arterial
 Middle meningeal a.

Lucid interval (50%)
MR appearance of intracerebral hemorrhage
The physics of MR imaging of hemorrhage is complex
The MR signal intensity of hemorrhage is dependent on both
the chemical state of the iron atoms within the hemoglobin
molecule
 The integrity of the red blood cell membrane.
 Iron can be either diamagnetic or paramagnetic, depending on
the state of its outer electron orbitals.
[MRI Clinics, 14:127, 2006]
 MR:


 Equally sensitive as CT in hyperacute phase
 More sensitive than CT in subacute and chronic phases
MRI - hemorrhage
CT
T1
T2
4. Early imaging finding of infarction
Acute infarcts can be seen as
early as < 6hrs from onset on CT
MR appearance of intracerebral hemorrhage
The physics of MR imaging of hemorrhage is complex
The MR signal intensity of hemorrhage is dependent on both
the chemical state of the iron atoms within the hemoglobin
molecule
 The integrity of the red blood cell membrane.
 Iron can be either diamagnetic or paramagnetic, depending on
the state of its outer electron orbitals.
[MRI Clinics, 14:127, 2006]
 MR:


 Equally sensitive as CT in hyperacute phase
 More sensitive than CT in subacute and chronic phases
5. Intramedullary spine lesions
Spinal Canal
Intramedullary
-Metastatic disease
-Astrocytoma
-Demyelination
-Ependymoma
-Myelitis
-Contusion
-Lymphoma
Mnemonic for above:
i MADE my MCL tear
IntraduralExtramedullary
-Neurofibroma
-Meningioma
-Schwannoma
-Lymphoma
-Subarachnoid
metastasis
Extradural
-Disc herniation's
-Trauma
-Hematoma
-Schwannomas
-Metastatic and
primary bone
tumors
M = Metastasis





Focal cord enhancing
lesion with extensive
edema
Cord expansion
Hematogenous
dissemination
Lung > breast
Other lesion (brain 20%59%)
A - Astrocyoma - Tumor



Astrocyoma
Most common
intramedullary tumor in
children/young adults
Usually low grade (8090%)
D – Demyelinating - Inflammation




Demyelinating =
Multiple Sclerosis
Isolated spinal cord
disease (10-20%)
Cervical cord most
common
DDx- Neoplasm,
Idiopathic transverse
myelitis, infarction
Neuromyelitis optica
E - Ependyomoma - Tumor






Ependyomoma
Most common primary
cord tumor in adults
Well circumscribed
Tumoral cysts
Slow growing
Hemorrhage
M – Myelitis - Inflammation




Idiopathic transverse
myelitis
Inflammatory disorder
possibly associated with
previous viral infection
or vaccination
Involves both halves of
the cord (bilateral
sensory, motor and
autonomic dysfunction)
Demyelination
L - Lymphoma




Multiple locations of
involvement.
Extradural, osseous,
intramedullary,
intraduralextramedullary
NHL>>Hodgkin dx
Primary, hematogenous
metastatic or local
spread
6. Spinal cord met findings
Spinal Cord - Metastasis





Focal cord enhancing
lesion with extensive
edema
Cord expansion
Hematogenous
dissemination
Lung > breast
Other lesion (brain 20%59%)
Spinal Cord – Lymphoma (repeat
slide)




Multiple locations of
involvement.
Extradural, osseous,
intramedullary,
intraduralextramedullary
NHL>>Hodgkin dx
Primary, hematogenous
metastatic or local
spread
7. MS MRI findings
Multiple Sclerosis








Etiology – unknown – probable virus and/or
autoimmune mediated
Activated T cells attack myelinated axons
Age 20-40
M:F = 1:2
Caucasian most common
Most often occurs in temperate zones
Most common disabling CNS disease of young
adults; 1:1000 in Western world
“Dawson’s finger”
Multiple Sclerosis
DAWSON’s FINGERS
Multiple Sclerosis
1.
2.
3.
4.
5.
CVA vs. TIA
Contraindications to TPA
NIH Stroke scale uses
Locked in symptoms =?
Ischemic stroke treatment
1. CVA vs. TIA
***Consequences of CVA***


Infarct – cells directly around feeder vessel die,
central core of dead tissue
Penumbra
 Cells farther from core may have collateral circulation
 These cells don’t immediately die, can recover if blood flow
restored

Cerebral Edema
 Cytotoxic - failure of ATP transport of Ca and NA = cellular
swelling
 Vasogenic – increased permeability of vascular endothelial
cells, increased extracellular fluid volume
 Increased ICP (Decreased BF, mass effect, displaced brain
tissue, herniation)
***TIA***
“Transient ischemic attack (TIA): a transient episode of
neurological dysfunction caused by focal brain, spinal
cord, or retinal ischemia, without acute
infarction.”
 50% with a TIA have a stroke in 48 hours
 10-15% of patients with TIA have a stroke in 3 months
 Types

 Large artery low flow
 Embolic
 Lacunar
Anterior Cerebral Artery
Contralateral hemiparesis LEG > arm
 Akinetic mutism
 Behavioral or memory disturbance
 Dysarthria
 Conjugate eye deviation towards lesion

Middle Cerebral artery
Contralateral hemiplegia or hemiparesis ARM
> leg
 Contralateral hemisensory syndrome
 Homonymous hemianopsia
 Contralateral lower facial weakness
 Speech or language abnormality

Posterior Cerebral Artery
Contralateral Homonymous Hemianopsia
 VF deficits
 Parasthesias of face, limb, trunk

Lacunar Strokes

Pure motor hemiplegia





Contralateral face and arm>leg weakness
Possible mild dysarthria
No vision, language, or sensory disturbance
Lesion usually in the contralateral posterior limb of
the internal capsule
Pure sensory stroke
 Contralateral face, arm, trunk, and leg numbness,
paresthesias, and reduction of pain temperature
 Lesion usually in the contralateral VPL thalamic
nucleus.
2. Contraindications to TPA
***Acute Treatment***

TPA in acute ischemic stroke – in acute ischemic stroke
 Alterplase- binds to fibrin and converts plasminogen to plasmin promoting
fibrinolysis

Inclusion Criteria
 Diagnosis of ischemic stroke causing measurable neurological deficit
 Onset of symptoms < 4.5 h before beginning treatment
 Aged > 18 years

Exclusion Criteria
 Significant head trauma or prior stroke in previous 3 mo
 Symptoms suggest subarachnoid hemorrhage or history of previous





intracranial hemorrhage
Intracranial neoplasm, arteriovenous malformation, or aneurysm
Recent intracranial or intraspinal surgery
Elevated blood pressure (systolic > 185 mm Hg or diastolic > 110 mm Hg)
Active internal bleeding or acute bleeding diathesis
CT demonstrates multilobar infarction (hypodensity > ⅓ cerebral
hemisphere)
3. NIH Stroke scale uses
***NIHSS***
15 item scale to measure neurologic
impairment
 Used in clinical trials and clinical care
 Predictive of outcome
 http://www.ninds.nih.gov/doctors/NIH_Stroke_
Scale.pdf

4. Locked in symptoms =?
***Vertebrobasilar Artery***

“Locked-in” syndrome
 Characterized by aphonia, quadriplegia, and
preserved eye movements (except for horizontal
movements which are occasionally affected)
 Wakefulness is maintained
5. Ischemic stroke treatment
***Acute Treatment***


ABCs
American Heart and Stroke Association Recommendations
 Treat hypoxia (oxygen saturation < 94%), but no routine
supplemental O2
 Manage blood pressure if the patient has malignant Hypertension







(220/120)
Do NOT give empiric prophylactic treatment for seizure prevention
Give aspirin, but not if the patient has received tPA
Do NOT anticoagulate most patients in the acute phase, whether or
not they have received tPA, because of risk of serious bleeding
Treat hyperthermia temp >38 degrees Celsius
Keep glucose in the range of 140 to 180 mg/dL
Monitor neuro checks
Monitor for signs of aspiration
1.
2.
3.
4.
Most common cause
Diagnosis and/or workup
Goal for BP treatment
Aneurysm screening recommendations
1. Most common cause of
hemorrhagic stroke
***Causes***
Hypertension = Most common cause
 Aneurysms/Vascular Malformations
 Cerebral Amyloid Angiopathy
 Neoplasms
 Vasculitis
 Systemic Coagulation disorders
 Antithrombotic therapy

EXAM!!!!
2. Diagnosis and/or workup of
hemorrhagic stroke
Radiologic Diagnosis of hemorrhagic
stroke

Head CT – noncontrast = GOLD STANDARD





Provides size and location
Presence of surrounding edema
Shows shifts of brain contents
Hyperacute blood appears hyperdense
MRI
 100% sensitivity and accuracy by experienced
readers

CTA/MRA – useful screening test for vascular
malformations and aneurysms
Laboratory Workup

Laboratory
 Blood Glucose Level
 CBC
 BMP (platelets)
 PT/PTT
 Cardiac enzyme levels
 Toxicology screen/Pregnancy test
 Blood Alcohol levels
3. Goal for BP treatment of
hemorrhagic stroke
***Acute Management***

Blood Pressure
 HTN can worsen bleeding and cause hemorrhage
expansion
 If presenting SBP 150-220 mm Hg blood pressure
goal is SBP 140 mm Hg
 Useful IV agents:
○ Labetalol, nicardipine, esmolol, enalapril, hydralazine,
nitroprusside, nitroglycerine
4. Aneurysm screening recommendations
***Risks Factors and Prevention***








Hypertension
Smoking/ETOH
Sympathomimetic drug use (cocaine)
History previous SAH
Family history of aneurysms or SAH
Ehlers-Danlos Syndrome
Polycystic Kidney Disease
**CTA/MRA - Offer non-invasive screening to
patients with first degree relative with aSAH or
hx SAH**
EXAM!!!
Radiologic Diagnosis

Head CT – noncontrast = GOLD STANDARD





Provides size and location
Presence of surrounding edema
Shows shifts of brain contents
Hyperacute blood appears hyperdense
MRI
 100% sensitivity and accuracy by experienced
readers

CTA/MRA – useful screening test for
vascular malformations and aneurysms