Back into circulation from venous sinus at the fourth

 Back into circulation from venous sinus
 At the fourth ventricle circulation continues down spinal cord
ARACHNOID SPACE
 Skull – dura mater (periosteal layer – meningeal layer) – arachnoid membrane – arachnoid space – pia mater –
brain parenchyma
 Arachnoid space contains blood vessels which travel deep between brain sulci that provides glucose
 Pia mater, arachnoid membrane, dura mater = 3 layers of meninges
o Pain sensitive – especially dura mater
 Subarachnoid space – vasculature then CSF
o Bacteria from CSF use glucose in area for energy
o Vasculature respond to bacteria & increase vessel wall permeability
o Decrease in perfusion pressure/possible subsequent ischemia
o Increase in adhesion protein to allow leukocytes to invade
o Endothelial damage in response to cytokine-mediated inflammation
o Neutrophils enter due to vascular permeability and protein adhesion – leads to inflammation – leads to
meningitis
o Macrophages enter causing inflammation
o Increase in vascular permeability = water/protein enter subarachnoid space – causes cerebral edema
leading to increased cranial pressure
 Lumbar puncture for suspected meningitis = bacteria, increased proteins, increased neutrophils, decreased
glucose
 Classic Signs/Symptoms: fever, headache, photophobia, N/V, neck stiffness
CLINICAL MANIFESTATIONS OF MENINGITIS
 Classic triad: headache, fever, nuchal rigidity (neck stiffness)
 Other symptoms: photophobia, phonophobia
 Meningoencephalitis: altered mental state, seizures
MENINGITIS DIAGNOSIS & TREATMENT
 Diagnosis:
o Physical: Kernig’s sign (severe stiffness of hamstrings = inability to straighten leg when hip is flexed to 90
degrees), Brudzinski’s sign (severe neck stiffness causes hips & knees to flex when neck is flexed)
o Lumbar puncture: measures pressure, analyze CSF for WBCs, protein, glucose
o Polymerase Chain Reaction (PCR): identify specific causes of meningitis (HIV, enteroviruses, HSV,
tuberculosis)

 May use specific test is cause identified – Western blot for Borrelia burgdorferi, thin blood smear
for malaria
 Treatment:
o Bacterial: steroids followed by antibiotics to prevent massive injury to leptomeninges from inflammation
that can be caused as antibiotics destroy bacteria
o Drugs aimed at specific causes: antivirals, antibiotics, antifungals, antiparasitic
o Prevention: vaccines for some causes such as Neisseria meningitis, mumps, disseminated tuberculosis
o Prophylactic antibiotics: avoid outbreaks of bacterial meningitis
CNS ISCHEMIA
TRANSIENT ISCHEMIC ATTACK (TIA)
 Episode of neurological dysfunction without infarction (reversible ischemia)
 Increases risk for future stroke
 Associated with sudden onset syncope, amnesia, seizures
 Risk factors: HTN, atherosclerosis, DM, obesity, hypercoagulable states, amyloid angiopathy, afib, MI, hx TIA,
valvular disease
 Patho:
o Divided based on anterior/posterior circulation
 Posterior: Posterior cerebral artery, superior cerebral artery, posterior inferior cerebellar artery,
vertebral artery, basilar artery
 Anterior: branches of middle cerebral artery, anterior cerebral artery, internal carotid artery
o Anterior Circulation: internal carotid first – Circle of Willis – branches into anterior towards brain
between two hemispheres – splits into middle cerebral artery on side of brain
 Branch from internal carotid to ophthalmic artery that innervates eyeball – can present with
ocular blindness if TIA here
o Posterior Circulation: Vertebral arteries – Posterior inferior cerebella artery (PICA) – basilar artery –