Edema, Cerebral Intracranial Shifts, and Herniations I. Anatomic Considerations 1. Know anatomic relationships among medial temporal lobe, tentorium cerebelli, brainstem, upper CNs, and vertebro-basilar artery system (posterior circulation) 2. Brain restricted by skull and two dural reflections Falx cerebri: incomplete partition separating hemisphere in sagittal plane, stopping just above corpus callosum Tentorium cerebelli: horizontal reflection which lies on superior surface of cerebellum; separates supra- from infra-tentorial spaces -open in ventral midline to allow midbrain to pass through (tentorial notch) -each free edge lies adjacent to either side of midbrain 3. Brain itself not readily compressible Small increases in volume of brain may be tolerated since theres some room for expansion from compression of ventricles and subarachnoid space Large increases in volume cant be tolerated w/o serious consequences Compromise of adjacent tissue from rapid expansion in one part of brain Local expansionlocal pressurepressure gradientsshifts of tissue (deformation of brain substance) Structures at distance from main forcus of a lesion can also be compromised 4. Blood-brain-barrier CNS capillary endothelial cells linked by tight jxns, not fenestrated Endothelial pinocytic activity limited under normal conditions Most substances dont pass readily from blood vessels into brain parenchyma II. Brain Edema Edema: Increase in volume and weight of brain due to fluid accumulation Common complication of many kinds of intracranial lesions Serious b/c produces additional in volume over and above that resulting from lesion itself Vasogenic Edema Results from vascular permeability due to: a) destruction of vessels (eg trauma, hemorrhage) b) pinocytic activity c) growth of capillaries that dont have competent BBB (eg tumor vessels, either in CNS or metastatic, or in granulation tissue) Extent of edema influenced by a) mean systemic BP b) duration of incompetence of BBB Edema arising focally (eg tumor, infarct, local infection) can spread through CNS Movt through white matter occurs more easily than through gray matter since extracellular space irregular and wider (up to 800 ) in white Fluid through gray matter restricted b/c extracellular space narrower (100-200 ) and there are many synaptic jxns Cytotoxic Edema Fluid is plasma filtrate containing variable amounts of plasma proteins Swelling of cellular elements in presence of intact BBB Eg. consequences of triethyl tin (cosmetics) and hexachlorophene (disinfectant) toxicity Both cause accumulation of fluid w/in lamellae of myelin sheaths, incl splits and blebs in myelin Fluid is ultrafiltrate and doesnt contain plasma proteins In animal models of ischemic brain damage Early changes incl in water content then swelling of astrocyte processes After several hrs breakdown of BBB occurs Early edema after ischemic injury is cytotoxic, and later edema has vasogenic component
Edema of ischemic infarcts shows both types of edema
III. Increased ICP ICP normally maintained by maintaining intracranial volume through cerebral blood flow regulation and by balance of cerebrospinal fluid production and resorption Normal ICP limit falls below 15 mmHg Several causes of ICP: Mass lesions Tumors, hematomas, abscesses, granulomas Brain edema due to incompetence of BBB in these lesions may further ICP Edema a) focal: most common, occurs about lesions where theres BBB breakdown b) generalized cerebral edema: rare, but observed in several settings Pseudotumor cerebri: seen in young women, associated w/ obesity and endocrine dysfcn; headache and papilledema (if untreatedvisual field defects and blindess) Reyes syndrome Viral encephalitis Diabetic ketoacidosis: rarely Vascular changes a) Compression of jugular vv intracranial blood volume and ICP Compression of abdominal vv by Valsalva maneuver intraspinal pressure Used in testing patency of subarachnoid space, since w/ cervical or thoracic mass lesion, Valsalva produces quick rise in lumbar pressure, measured at LP, but jugular compression wont If block is partial, slow rise after jugular compression may be seen b) Hypercapneaintracranial vasodilatation ICP seen in some pts w/ pulmonary dz may be due in part to vasodilatation from CO2 retention c) Head trauma sometimes accompanied by loss of normal vasoregulation of intracranial circulationuncontrolled vasodilatation this complication more prevalent in children and leads to ICP loss of vasoregulation usu transient but reqs treatment to prevent irreversible brain damage CSF Blockage of CSF pathways ICP Removal of CSF by LP transiently ICP Serum osmolality Brain is in osmotic EQ w/ blood a) hypo-osmolal states (eg water intoxication) brain water and brain volume Sx: headache, seizures, eventually coma can occur w/ fall from normal 310 milliosmoles (mosm) of serum to 260 mosm b) hyper-osmolal statesCNS dehydration When serum osmolality rises to ~380 mosm, dehydration and brain shrinkage may produce mechanical distortion w/ tearing of blood vessels This complication important in dehydrated infants or those fed inadvertently w/ too much salt in formula Rare in adults: seen only in severe dehydration or uremia Continuous pressure measurements in pts w/ ICP demonstrated ICP doesnt remain constant but that there are episodic increases reaching over 50 mmHg and lasting 5-20 mins Plateau waves: elevations reflecting hyperemia in cerebral blood volume accompanies plateau waves waves may be associated w/ transient worsening of neurologic deterioration Brain is intolerant of rapid volume changes but can adjust to slow changes slowing growing lesions (eg meningiomas) may reach substantial size w/o producing ICP however, brain adjacent to such a lesion will be compressed and gliotic IV. Pathologic Consequences of Increased ICP A. Generalized in intracranial volume ICP (eg pseudotumor cerebri) Sx: headache, nausea, vomiting, papilledema, and 6th nerve palsy (false localizing sign, rare) In pseudotumor cerebri, theres no obstruction to CSF flow nor is regulation of cerebral blood flow disturbed Brain volume diffuselyshifts in brain substance usu dont occur
B. Shifts occur when pressure gradients develop w/in CNS Local in pressure due to in volume of mass cause lesions shifts away from lesion Areas remote from and adjacent to lesion may suffer distortion If distortion severe enough to interfere w/ blood flow, tear vessels, or compress CNS fiber pathways or CNs, clinically significant effects occur Herniations are the most serious CNS distortions: 1. cingulate Lateral hemispheric lesion will shift that hemisphere medially, pushing ipsi cingulated gyrus under free edge of falx cerebri May compress internal cerebral vein and ipsi anterior cerebral artery 2. uncal With supratentorial lesions, esp those in temporal and lateral parietal lobes, increased pressed is directed medially and downward, forcing most medial part of temporal lobe (uncus and hippocampal gyrus) over free edge of tentorium cerebelli Ipsi IIIrd nerve compressed by uncus against tentorial edge or anteriorly Ipsi papillary dilatation (one of earliest signs of uncal herniation) eventually against supraclinoid ligament to ipsi oculomotor palsy Herniating uncus push against midbrain, compress ipsi cerebral peduncle or Hemorrhage and pressure necrosis of peduncle force contra cerebra peduncle against contra free edge of tentorium Ipsilateral peduncular compression Hemiparesis or hemiplegia on side contra lesion Hemiparesis or hemiplegia ipsi to lesion Ischemic necrosis in arterial supply: infarcts of calcarine cx produce hemianopsia, and infarcts of posterior thalamus may also occur Increasing ICP and further herniationpressure transmitted to middle and Ischemic changes due to vascular compression lower brain stem levelsstem buckles Hemorrhages (Duret): predominates in midsagittal region; arterial, resulting from stretching of perforating vessels of stem Clinical signs referable to brain stem compromise during herniation progress rostralcaudal Ipsi papillary dilatation usu occurs first (midbrain) Disappearance of oculcephalic and oculovestibular reflexes indicates pontine dysfcn Coma develops as midbrain and pontine reticular formation compromised In late stages, eye signs and pyramidal tracts signs bilateral Supratentorial lesionsdownward shift of hemisphere, first compressing diencephalons, then forcing midbrain down through tentorial notch, and eventually distorting pons and medulla Mass lesions in frontal, parietal, or occipital lobes or extracerebral lesions at vertex may cause this In dzs such as Reyes syndrome or in trauma w/ loss of vasoregulation, hemispheric white matter may swell diffusely, faster than brain stem, producing downward pressure gradient Progression of signs reflects rostralcaudal progression of herniation Diencephalic signs Decreasing alertness progressing to stupor or coma (upper reticular formation) Small pupils Babinski reflexes Cheyne-Stokes breathing Decorticate posturing Midbrain signs Moderate papillary dilatation Dysconjugate eye movts Hyperventilation decerebration Contra peduncular compression (Waltman-Kernohans notch) Ipsi posterior cerebral artery compression
3. central
4. cerebellar tonsillar
loss of oculocephalic and oculovestibular reflexes shallow, irregular breathing flaccidity of limbs pupils in midposition and unresponsive Medullary signs irregular respiration apneic periods tachy- or bradycardia hypotension this is a terminal stage Displaced downward through foramen magnum can be seen as late stage of uncal or central herniation may result from rapidly expanding cerebeallar lesions tonsils compressed against margins of foramen magnum, causing tonsillar necrosis herniating tonsils squeeze medulla, producing medullary paralysis and death (loss of consciousness, bradycardia, irregular respirations or apneic periods, hypotension) cerebellar masses may produce signs of lower midbrain and pontine compression
Pontine and upper medullary signs
V. Trea...