Block 2

Question 1

proposed a clinical
classification utilizing both the temporal pattern of
child’s headache plotted against its severity over
time.

Answer 1

Winner and Rothner

Question 2

Single event with no history of previous similar

event.

Answer 2

Acute Headache

Question 3

Periodic headaches that are separated by painfree

intervals

Answer 3

Acute Recurrent Headache

Question 4

Ex. migraine

Answer 4

Acute Recurrent Headache

Question 5

Headaches that worsen in frequency and severity

over time.

Answer 5

Chronic Progressive Headache

Question 6

The progression may be rapid or slow

Answer 6

Chronic Progressive Headache

Question 7

May be accompanied by symptoms and signs of
increased intracranial pressure or progressive
neurologic disease

Answer 7

Chronic Progressive Headache

Question 8

The neurologic exam is usually abnormal

Answer 8

Chronic Progressive Headache

Question 9

Organic process is usually present

Answer 9

Chronic Progressive Headache

Question 10

Chronic Progressive Headache is also known as?

Answer 10

Also known as tension-type headaches,
muscle contraction headaches, chronic daily
headaches

Question 11

Generalized or localized

Answer 11

Acute Headache

Question 12

Maybe associated with neurologic symptoms and
signs or seen in the absence of neurologic
symptoms

Answer 12

Acute Headache

Question 13

Intracranial Sources of Headache Pain

Answer 13

1. Cerebra and dural arteries
2. Dura mater at the base of the brain
3. Large veins and venous sinuses
4. Blood vessels

Question 14

Main pain-sensitive structures inside the skull

Answer 14

Blood vessels

Question 15

Mechanisms of pain from the blood vessels:

Answer 15

1. Vasodilation
2. Inflammation
3. Traction-displacement

Question 16

Mechanism of pain transmission in intracranial source of headache pain

Answer 16

• Pain transmission from supratentorial intracranial
vessels is via Trigeminal nerve (specifically V1-
ophthalmic, which results in referred pain)
• Pain transmission from infratentorial vessels is by
the first 3 cervical nerves.

Question 17

Extracranial sources of headache pain

Answer 17

1. Cervical Roots
2. Cranial Nerves
3. Extracranial arteries
4. Muscles attached to the skull
5. Periosteum/ sinuses

Question 18

Neurological injury caused by the occlusion or

rupture of cerebral blood vessels

Answer 18

Stroke

Question 18

Neurological injury caused by the occlusion or

rupture of cerebral blood vessels

Answer 18

Stroke

Question 19

Two categories of stroke in children

Answer 19

1. Perinatal stroke

2. Childhood stroke

Question 20

MENINGITIS

Classified into 2 syndromes:

Answer 20

1. Septic or Purulent meningitis

2. Aseptic meningitis

Question 21

bacterial or fungal.

Answer 21

Septic or Purulent meningitis

Question 22

viral, spirochetal, protozoal, metazoal,

neoplastic, or other non-septic causes.

Answer 22

Aseptic meningitis

Question 23

Refers to the inflammation of the
leptomeninges (pia and arachnoid), the
connective tissue layers in close proximity to
the surface of the brain.

Answer 23

Leptomeningitis

Question 24

Bacterial organisms reach the meningeal | region by one of 4 routes:

Answer 24

1. Direct hematogenous spread. 2. Passage through the choroid plexus (infection is already inside the brain). 3. Rupture of superficial cortical abscesses. 4. Contiguous spread of an adjacent infection

Question 25

 Occurs during bacteremia  Through the passive transfer of organism by infected leukocytes.  Through damaged or malformed blood vessels or because of neurosurgical procedures.  In cases of neurosurgical procedures

Answer 25

Direct Hematogenous Spread

Question 26

 Abscess, osteomyelitis (especially in the temporal bone) of the skull or the head and spine.  Otitis media (mastoiditis), sinusitis  Developmental anomalies and penetrating injuries of the skull.  Develop after bacterial attachment and invasion of the nasopharyngeal mucosa.

Answer 26

Contiguous spread of adjacent infection:

Question 27

Bacterial organisms secrete IgA | proteases that neutralize IgA.

Answer 27

1. S.pneumoniae 2. H. influenza 3. N. meningitides

Question 28

Blood Brain Barrier composed of:

Answer 28

1. Arachnoid membrane 2. Choroid plexus epithelium 3. Endothelial cells of the cerebral microvasculature

Question 29

BBB is disrupted by?

Answer 29

nitric oxide and metabolites | of the arachidonic pathway

Question 30

Upon entering the ______, bacteria encounter few host defenses because it lacks antibody complement and opsonic activity.

Answer 30

CSF

Question 31

hyperemia of the meningeal vessels.

Answer 31

1st stage

Question 32

migration of neutrophils into the | subarachnoid space.

Answer 32

2nd stage

Question 33

rapidly increases over hours and extends into the sheaths of blood vessels and along cranial and spinal nerves PMNs that contain phagocytized bacteria predominate

Answer 33

Subarachnoid exudate

Question 34

begin to degenerate and | are removed by macrophages.

Answer 34

Neutrophil leukocytes

Question 35

Fibrinogen and other blood proteins are exuded, and more plasma cells appear

Answer 35

(2nd week)

Question 36

The exudate beneath the arachnoid consists of | an outer layer of?

Answer 36

neutrophils and fibrin

Question 37

The exudate beneath the arachnoid consists of an inner layer composed of?

Answer 37

lymphocytes, macrophages, and plasma cells.

Question 38

Endothelial cells swell, proliferate, and crowd into the vessel lumen in?

Answer 38

48 to 72 hours

Question 39

________ and ________ develop that | partially or totally occlude the lumen.

Answer 39

Focal necrosis and mural thrombi

Question 40

In _______, venous thrombosis is much more frequent than arterial thrombosis.

Answer 40

bacterial meningitis

Question 41

Venous thrombosis is common in?

Answer 41

subdural empyema

Question 42

________ persist for months

Answer 42

Lymphocytes, plasma cells and macrophages

Question 43

GOLD STANDARD in diagnosis meningitis

Answer 43

CSF culture by doing Lumbar Puncture

Question 44

Are soluble proteins that are released by host cells in response to bacterial products such as endotoxin, cell walls, and toxins.

Answer 44

Cytokines

Question 45

In excess amounts they contribute to | parenchymal injury because it will:

Answer 45

1. Directly affect the function of the endothelial cells. 2. Increase the blood-brain barrier permeability. 3. Decrease autoregulation of cerebral blood flow. 4. Induce cytotoxic edema. 5. Induce recruitment of leukocytes into the infected compartment.

Question 46

Proinflammatory cytokines

Answer 46

1. Tumor necrosis factor-alpha (TNF-a) 2. Interleukine-1B (IL-1B) 3. Interleukin-6 (IL-6) 4. Interleukin-8 (IL-8)

Question 47

Anti-inflammatory cytokines

Answer 47

1. IL-10 | 2. Transforming growth factor B (TGF-B)

Question 48

 Increases the permeability of the blood-brain barrier.  Induces cell lysis.  Mediates myelin and oligodendrocyte damage.  If you have destruction of myelin, this will affect the action of your axons and will lead to motor dysfunctions.

Answer 48

TNF-a

Question 49

 Highly potent inducer of neutrophil accumulation and procoagulant (can cause thrombosis, infarction and stroke-like phenomenon).  Stimulates the release of other cytokines such as TNF and IL-6 and of hypothalamic corticotrophin-releasing factor

Answer 49

IL-1B

Question 50

 a pyrogen |  Plays a role in the induction and propagation of inflammatory responses

Answer 50

IL-6

Question 51

 A leukocyte chemotactic agent that promotes leukocyte adherence ( increase in meningococcal meningitis)  Downregulates inflammation and may contribute to chronicity of disease

Answer 51

IL-8

Question 52

 Downregulate inflammation and may contribute to chronicity of disease.  Not present in serum but is elevated in CSF in the first 48 to 72 hours of viral meningitis

Answer 52

IL-10

Question 53

hydrocephalus

Answer 53

Fibrinopurulent exudate accumulates in large quantities → obstruction of the foramina of Luschka and Magendie or the aqueduct of Sylvius → hydrocephalus

Question 54

Result from inflammation of exudate in the subarachnoid space around the brainstem and over the cerebral convexity.

Answer 54

Communicating Hydrocephalus

Question 55

- ---Induced by components of the neutrophil membrane | - ---Can depolarize neuronal membranes and lead to seizure activity

Answer 55

Brain edema

Question 56

2 types of brain edema in meningitis

Answer 56

1. Cytotoxic | 2. Vasogenic

Question 57

→ Marked by increased brain water, cellular swelling. → Increased intracellular sodium. → Loss of intracellular potassium.

Answer 57

Cytotoxic edema

Question 58

→ Caused by opening of tight junctions between cerebral capillary endothelial cells → Can result from the presence of bacteria as well as inflammation.

Answer 58

Vasogenic edema

Question 59

Early signs of bacterial meningitis:

Answer 59

Low-grade fever, poor feeding, somnolence, irritability

Question 60

Later signs of bacterial meningitis:

Answer 60

vomiting, lethargy, seizure

Question 61

 Streptococcal meningitis

Answer 61

78% -

Question 62

 H. influenza meningitis

Answer 62

44% -

Question 63

 S. pneumonia

Answer 63

25% -

Question 64

 Meningococcal infections

Answer 64

10% -

Question 65

Complications – Acute Bacterial Meningitis

Answer 65

1. Ventriculitis 2. Subdural effusion/subdural empyema 3. Electrolyte disturbance 4. Recurrent bacterial meningitis

Question 66

 Infections of the ventricular system can be primary  Can develop secondary to the spread of organism from the subarachnoid space caused by the flow of CSF or by migration of bacteria

Answer 66

Ventriculitis

Question 67

 Caused by increased efflux of intravascular fluids  Consequence of thrombophlebitis of the veins bridging the subdural space  Abnormal vascular permeability at the arachnoid-dura infertace  Spread of infection from arachnoditis

Answer 67

Subdural effusion / subdural empyema

Question 68

 Most common cause of subdural effusion/ subdural empyema:

Answer 68

H. influenza (45%)  Pneumococcus (30%)  Meningococcus (9%)

Question 69

 Management for Subdural effusion / subdural empyema:

Answer 69

1. Conservative treatment of subdural effusions. 2. Multiple subdural aspirations or surgical intervention no longer recommended.

Question 70

 Indications for subdural tap

Answer 70

1. Patients suspected of subdural empyema. 2. If the effusion becomes hemorrhagic. 3. If large enough to cause a significant ventricular shift

Question 71

Hyponatremia is secondary to:

Answer 71

1. Inflammation 2. Syndrome of inappropriately high secretion of antidiuretic hormone (SIADH) 3. Increased release of atrial natriuretic peptide.

Question 72

Gold standard for the diagnosis of bacterial meningitis –

Answer 72

identification by culture and gram | stain of CSF

Question 73

Expected CSF findings:

Answer 73

1. Fluid is cloudy, increased pressure. 2. Acute stage: PMNs, mononuclear later stage. 3. Cell count: 1,000 to 10,000 per uL. 4. Glucose decreased (bacterial/TB) o Less than 40% (bacterial). 5. Protein is increased 100 mg/dl and higher.