increased intracranial pressure patrick c.j. ward, m.d. professor & head dept. of anatomy,...

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