Block 2 Flashcards
proposed a clinical
classification utilizing both the temporal pattern of
child’s headache plotted against its severity over
time.
Winner and Rothner
Single event with no history of previous similar
event.
Acute Headache
Periodic headaches that are separated by painfree
intervals
Acute Recurrent Headache
Ex. migraine
Acute Recurrent Headache
Headaches that worsen in frequency and severity
over time.
Chronic Progressive Headache
The progression may be rapid or slow
Chronic Progressive Headache
May be accompanied by symptoms and signs of
increased intracranial pressure or progressive
neurologic disease
Chronic Progressive Headache
The neurologic exam is usually abnormal
Chronic Progressive Headache
Organic process is usually present
Chronic Progressive Headache
Chronic Progressive Headache is also known as?
Also known as tension-type headaches,
muscle contraction headaches, chronic daily
headaches
Generalized or localized
Acute Headache
Maybe associated with neurologic symptoms and
signs or seen in the absence of neurologic
symptoms
Acute Headache
Intracranial Sources of Headache Pain
- Cerebra and dural arteries
- Dura mater at the base of the brain
- Large veins and venous sinuses
- Blood vessels
Main pain-sensitive structures inside the skull
Blood vessels
Mechanisms of pain from the blood vessels:
- Vasodilation
- Inflammation
- Traction-displacement
Mechanism of pain transmission in intracranial source of headache pain
• 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.
Extracranial sources of headache pain
- Cervical Roots
- Cranial Nerves
- Extracranial arteries
- Muscles attached to the skull
- Periosteum/ sinuses
Neurological injury caused by the occlusion or
rupture of cerebral blood vessels
Stroke
Neurological injury caused by the occlusion or
rupture of cerebral blood vessels
Stroke
Two categories of stroke in children
- Perinatal stroke
2. Childhood stroke
MENINGITIS
Classified into 2 syndromes:
- Septic or Purulent meningitis
2. Aseptic meningitis
bacterial or fungal.
Septic or Purulent meningitis
viral, spirochetal, protozoal, metazoal,
neoplastic, or other non-septic causes.
Aseptic meningitis
Refers to the inflammation of the
leptomeninges (pia and arachnoid), the
connective tissue layers in close proximity to
the surface of the brain.
Leptomeningitis
Bacterial organisms reach the meningeal
region by one of 4 routes:
- Direct hematogenous spread.
- Passage through the choroid plexus
(infection is already inside the brain). - Rupture of superficial cortical abscesses.
- Contiguous spread of an adjacent infection
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
Direct Hematogenous Spread
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.
Contiguous spread of adjacent infection:
Bacterial organisms secrete IgA
proteases that neutralize IgA.
- S.pneumoniae
- H. influenza
- N. meningitides
Blood Brain Barrier composed of:
- Arachnoid membrane
- Choroid plexus epithelium
- Endothelial cells of the cerebral
microvasculature
BBB is disrupted by?
nitric oxide and metabolites
of the arachidonic pathway
Upon entering the ______, bacteria encounter few host defenses because it lacks antibody complement and opsonic activity.
CSF
hyperemia of the meningeal vessels.
1st stage
migration of neutrophils into the
subarachnoid space.
2nd stage
rapidly increases over
hours and extends into the sheaths of blood vessels and along cranial and spinal nerves PMNs that contain phagocytized bacteria predominate
Subarachnoid exudate
begin to degenerate and
are removed by macrophages.
Neutrophil leukocytes
Fibrinogen and other blood proteins are exuded, and more plasma cells appear
(2nd week)
The exudate beneath the arachnoid consists of
an outer layer of?
neutrophils and fibrin
The exudate beneath the arachnoid consists of an inner layer composed of?
lymphocytes, macrophages, and plasma cells.
Endothelial cells swell, proliferate, and crowd into the vessel lumen in?
48 to 72 hours
________ and ________ develop that
partially or totally occlude the lumen.
Focal necrosis and mural thrombi
In _______, venous thrombosis is much more frequent than arterial thrombosis.
bacterial meningitis
Venous thrombosis is common in?
subdural empyema
________ persist for months
Lymphocytes, plasma cells and macrophages
GOLD STANDARD in diagnosis meningitis
CSF culture by doing Lumbar Puncture
Are soluble proteins that are released by host cells in response to bacterial products such as endotoxin, cell walls, and toxins.
Cytokines
In excess amounts they contribute to
parenchymal injury because it will:
- Directly affect the function of the endothelial cells.
- Increase the blood-brain barrier permeability.
- Decrease autoregulation of cerebral blood flow.
- Induce cytotoxic edema.
- Induce recruitment of leukocytes into the infected compartment.
Proinflammatory cytokines
- Tumor necrosis factor-alpha (TNF-a)
- Interleukine-1B (IL-1B)
- Interleukin-6 (IL-6)
- Interleukin-8 (IL-8)
Anti-inflammatory cytokines
- IL-10
2. Transforming growth factor B (TGF-B)
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.
TNF-a
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
IL-1B
a pyrogen
Plays a role in the induction and propagation of inflammatory responses
IL-6
A leukocyte chemotactic agent that promotes leukocyte adherence ( increase in meningococcal meningitis)
Downregulates inflammation and may contribute to chronicity of disease
IL-8
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
IL-10
hydrocephalus
Fibrinopurulent exudate accumulates in large quantities → obstruction of the foramina of Luschka and Magendie or the aqueduct of Sylvius → hydrocephalus
Result from inflammation of exudate in the subarachnoid space around the brainstem and over the cerebral convexity.
Communicating Hydrocephalus
- —Induced by components of the neutrophil membrane
- —Can depolarize neuronal membranes and lead to seizure activity
Brain edema
2 types of brain edema in meningitis
- Cytotoxic
2. Vasogenic
→ Marked by increased brain water, cellular swelling.
→ Increased intracellular sodium.
→ Loss of intracellular potassium.
Cytotoxic edema
→ Caused by opening of tight junctions between cerebral capillary endothelial cells
→ Can result from the presence of bacteria as well as inflammation.
Vasogenic edema
Early signs of bacterial meningitis:
Low-grade fever, poor feeding, somnolence, irritability
Later signs of bacterial meningitis:
vomiting, lethargy, seizure
Streptococcal meningitis
78% -
H. influenza meningitis
44% -
S. pneumonia
25% -
Meningococcal infections
10% -
Complications – Acute Bacterial Meningitis
- Ventriculitis
- Subdural effusion/subdural empyema
- Electrolyte disturbance
- Recurrent bacterial meningitis
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
Ventriculitis
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
Subdural effusion / subdural empyema
Most common cause of subdural effusion/ subdural empyema:
H. influenza (45%)
Pneumococcus (30%)
Meningococcus (9%)
Management for Subdural effusion / subdural empyema:
- Conservative treatment of subdural effusions.
- Multiple subdural aspirations or surgical
intervention no longer recommended.
Indications for subdural tap
- Patients suspected of subdural empyema.
- If the effusion becomes hemorrhagic.
- If large enough to cause a significant
ventricular shift
Hyponatremia is secondary to:
- Inflammation
- Syndrome of inappropriately high secretion of antidiuretic hormone (SIADH)
- Increased release of atrial natriuretic peptide.
Gold standard for the diagnosis of bacterial meningitis –
identification by culture and gram
stain of CSF
Expected CSF findings:
- Fluid is cloudy, increased pressure.
- Acute stage: PMNs, mononuclear later stage.
- Cell count: 1,000 to 10,000 per uL.
- Glucose decreased (bacterial/TB)
o Less than 40% (bacterial). - Protein is increased 100 mg/dl and higher.
