INCREASED INTRACRANIAL PRESSURE
Patrick C.J. Ward, M.D.
Professor & Head
Dept. of Anatomy, Microbiology & Pathology
January, 2008
INTRACRANIAL PRESSURE
• ULN: 200 mm H2O
• Cushion against brain injury during sudden movement
supplemented by the compressibility of veins
• Wide fluctuations limited by:
rigid calvarium (except in children)
blood / brain barrier
paucity of lymphatics
• Increased: mass effect (Pb), focal (neoplasia, etc.)
INCREASED INTRACRANIAL PRESSURE: CLINICAL
• Headaches
• Decreased LOC
• Bradycardia
• Papilledema
• Signs of uncal herniation
fixed pupil
ipsilateral paralysis
INCREASED INTRACRANIAL PRESSURE (ICP)
• Herniation
HERNIATION (1): GENERAL
• Unilateral space-occupying lesions such as:
tumor
abscess
hematoma
• Bilateral (diffuse):
cerebral edema
encephalitis
subarachnoid hemorrhage (SAH)
HERNIATION (2): TYPE / CONSEQUENCES
• Cingulate (subfalcine) compression of anterior cerebral artery
• Transtentorial (uncal) 3rd cranial nerve compressed
– ipsilateral papillary dilation– ipsilateral impairment of ocular movement
Kernohan’s notch (consequences ?) posterior cerebral artery (consequences ?) Duret hemorrhage
• Tonsillar (cerebellar)
Cooke Colour Atlas of Anatomy & Pathology, 1987.
INCREASED INTRACRANIAL PRESSURE (ICP)
• Herniation
• Cerebral edema
CEREBRAL EDEMA (1): BASIC
• Substituents of blood-brain barrier (BBB)
tight capillary endothelial junctions
capillary basement membranes
pericapillary astrocytic foot processes
CEREBRAL EDEMA (2): TYPES
• Vasogenic: localized
– cancer, abscesses, infarctions, contusions generalized
– lead poisoning, Reye syndrome
• Cytotoxic: ischemia H2O intoxication
• Interstitial (periventricular): hydrocephalus
REYE SYNDROME: PATHOLOGY
• LIVER: reversible. Bili, SGOT, FFA, BUN, NH4
microvesicular fatty change abnormal mitochondria (EM).
• CNS: cerebral edema without inflammation increased intracranial pressure herniation death in 10-40%
INCREASED INTRACRANIAL PRESSURE (ICP)
• Herniation
• Cerebral edema
• Hydrocephalus
HYDROCEPHALUS: VARIANTS
• Noncommunicating
• Communicating
• Ex-vacuo
• Overproduction
• Normal pressure
HYDROCEPHALUS: VARIANTS
• Non-communicating
HYDROCEPHALUS: NON-COMMUNICATING
• Congenital malformations aqueduct, Arnold-Chiari, Dandy-Walker
• Neoplasms ependymoma, medulloblastoma
• Inflammatory processes cerebral abscesses, CMID
• Hemorrhages parenchymal, intraventicular, epi-/subdural
CRANIOPHARYNGIOMA
• Derived from vistigia of Rathke pouch
• 1-5% of intracranial tumors
• Most are suprasellar. Slow growing.
• Bimodel age distribution (5-15, 60-70)
• Children: growth disturbances
• Adults: visual disturbances or diabetes insipidus
• Micro: nests of squamous cells, dystrophic ca++
HYDROCEPHALUS: VARIANTS
• Non-communicating
• Communicating
HYDROCEPHALUS: COMMUNICATING
• Post meningitic states (S. pneumoniae, tuberculosis)
• Subarachnoid hemorrhage
• Dural sinus thrombosis
• Some choroid plexus papillomas (overproduction)
HYDROCEPHALUS: VARIANTS
• Non-communicating
• Communicating
• Ex-vacuo
HYDROCEPHALUS: EX-VACUO
• Alzheimer disease
• Pick disease
HYDROCEPHALUS: VARIANTS
• Non-communicating
• Communicating
• Ex-vacuo
• Overproduction of CSF
HYDROCEPHALUS: OVERPRODUCTION OF CSF
• Choroid plexus papilloma
HYDROCEPHALUS: VARIANTS
• Non-communicating
• Communicating
• Ex-vacuo
• Overproduction
• Normal pressure
HYDROCEPHALUS: NORMAL PRESSURE
• Slowly evolving in the elderly
• Shunt ?
NORMAL PRESSURE HYDROCEPHALUS (NPH)
• Gait apraxia (slow, unsteady, wide-based)
so-called “magnetic gait”
difficulty in turning
• Urinary incontinence
• Dementia─multidimensional
Note: a form of communicating hydrocephalus
Lepsch, 2002
NPH: DIAGNOSTIC TRIAD
Gait apraxia
Urinary incontinence
Dementia
NPH: PATHOPHYSIOLOGY (1)
Gait apraxia
Urinary incontinence
• Epicenter: axons around dilated frontal horns
• Destination: legs, sphincters
• Lesion: stretching of axons
Dementia
NPH: PATHOPHYSIOLOGY (2)
Dementia
• Cause? increased intracranial pressure
• How? radial shearing forces on cortex compromise of microvasculature (?)
NPH: RADIOLOGY
• Ventricles larger than in Alzheimer disease
but without significant cortical atrophy
• Preservation of perihippocampal fissures
cf. Alzheimer disease (dilated)
• Hippocampus not atrophied
cf. Alzheimer disease (atrophied)
• Sylvian cisterns may be especially large
NPHN AD
NPH: FAVORABLE RESPONSE TO SHUNTING
• Presence of classic triad
especially when gait apraxia is primary symptom
• Opening pressure of CSF > 100 mm H20
continuous monitoring: pressure > 180 mm H20
• Enlarged ventricles with flattened sulci
• Small or absent perihippocampal fissures
Awasthi, 1998