INCREASED INTRACRANIAL PRESSURE Patrick C.J. Ward, M.D. Professor & Head Dept. of Anatomy, Microbiology & Pathology January, 2008

INTRACRANIAL PRESSURE ULN: 200 mm H 2 O Cushion against brain injury during sudden movement u supplemented by the compressibility of veins Wide fluctuations limited by: u rigid calvarium (except in children) u blood / brain barrier u paucity of lymphatics Increased: mass effect (Pb), focal (neoplasia, etc.)

INCREASED INTRACRANIAL PRESSURE: CLINICAL Headaches Decreased LOC Bradycardia Papilledema Signs of uncal herniation u fixed pupil u ipsilateral paralysis

INCREASED INTRACRANIAL PRESSURE (ICP) Herniation

HERNIATION (1): GENERAL Unilateral space-occupying lesions such as: u tumor u abscess u hematoma Bilateral (diffuse): u cerebral edema u encephalitis u subarachnoid hemorrhage (SAH)

HERNIATION (2): TYPE / CONSEQUENCES Cingulate (subfalcine) u compression of anterior cerebral artery Transtentorial (uncal) u 3 rd cranial nerve compressed –ipsilateral papillary dilation –ipsilateral impairment of ocular movement u Kernohan’s notch (consequences ?) u posterior cerebral artery (consequences ?) u 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) u tight capillary endothelial junctions u capillary basement membranes u pericapillary astrocytic foot processes

CEREBRAL EDEMA (2): TYPES Vasogenic: u localized –cancer, abscesses, infarctions, contusions u generalized –lead poisoning, Reye syndrome Cytotoxic: u ischemia u H 2 O intoxication Interstitial (periventricular): u hydrocephalus

REYE SYNDROME: PATHOLOGY LIVER: u reversible.  Bili,  SGOT,  FFA,  BUN,  NH 4 u microvesicular fatty change u abnormal mitochondria (EM). CNS: u cerebral edema without inflammation u increased intracranial pressure  herniation u 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 u aqueduct, Arnold-Chiari, Dandy-Walker Neoplasms u ependymoma, medulloblastoma Inflammatory processes u cerebral abscesses, CMID Hemorrhages u 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) u so-called “magnetic gait” u 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? u increased intracranial pressure How? u radial shearing forces on cortex u compromise of microvasculature (?)

NPH: RADIOLOGY Ventricles larger than in Alzheimer disease u but without significant cortical atrophy Preservation of perihippocampal fissures u cf. Alzheimer disease (dilated) Hippocampus not atrophied u cf. Alzheimer disease (atrophied) Sylvian cisterns may be especially large

NPH N AD

NPH: FAVORABLE RESPONSE TO SHUNTING Presence of classic triad u especially when gait apraxia is primary symptom Opening pressure of CSF > 100 mm H 2 0 u continuous monitoring: pressure > 180 mm H 2 0 Enlarged ventricles with flattened sulci Small or absent perihippocampal fissures Awasthi, 1998