Page 368 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)
P. 368

Cerebrospinal Fluid Pressure, Cerebral Edema
       After the the cranial bone sutures have fused,  Water can also accumulate in the interstitial
       the brain is confined within a rigid casing. Its  space when the blood–brain barrier is intact
       volume cannot expand and any intracranial  but the osmolarity of the interstitial space is
       compartments can get larger only at the ex-  higher than that of blood, for example, if there
       pense of other compartments (→ A1).  is a rapid fall in the concentration of blood sug-
    Systems  brain is open to the CSF space of the spinal  ar (during treatment of diabetes mellitus), of
         The cerebrospinal fluid (CSF) space of the
                                                      +
                                       urea (dialysis), or of Na (interstitial cerebral
                                       edema; → B3). In those conditions the in-
       cord via the foramen magnum. The intravascu-
                                       crease of interstitial space may be accompa-
       lar space is momentarily increased with each
    Neuromuscular and Sensory  the pulse a small volume of CSF escapes  sure (→ p. 356). An acute disorder of CSF drain-
                                       nied by cell swelling.
       systolic pulse wave, and synchronously with
                                        CSF congestion also increases cerebral pres-
       through the foramen magnum into the spinal
       CSF space, i.e., the intravascular space is in-
                                       age causes a rise in pressure that, via narrow-
                                       ing of the vessel lumen, impairs cerebral per-
       creased at the expense of the CSF space
       (→ A2).
                                       fusion (→ A4). Chronic drainage abnormality,
                                       by bringing about the death of neurons, i.e., a
         Similarly, an increase in interstitial or intra-
       cellular volume at first occurs at the expense
                                       decrease in intracellular space, will ultimately
       and the CSF space has collapsed, CSF pressure
                                        Tumors and bleeding (→ A3) take up intra-
                                       cranial volume at the expense of other com-
       quickly rises and there is a marked decrease
    10  of the CSF space. Once this reserve is used up  result in a decrease in cerebral mass (→ B5).
                                       partments, especially the CSF space.
       in cerebral perfusion (→ A3).
         Several forms of cerebral edema are distin-  Symptoms of increased CSF pressure. Due
       guished (→ B):                  to the increased cerebral pressure, lymph
         Cytotoxic edemas enlarge the intracellular  from the back of the eye can no longer flow to-
       space as a result of cell swelling (→ B1).  ward the intracranial space via the lymphatic
       Among causes are energy deficiency (e.g., due  canal at the center of the optic nerve. Lymph
                                   +
       to hypoxia or ischemia). Impairment of Na /  thus collects at the exit of the optic nerve and
        +
                              +
       K -ATPase raises the intracellular Na concen-  causes bulging of the papilla (papilledema;
                              +
       tration and decreases intracellular K concen-  → C1). Other consequences of increased CSF
       tration. Subsequent depolarization leads to  pressure are headache, nausea, vomiting, dizzi-
        –
       Cl entry and cell swelling (→ p.10).  ness, impaired consciousness (e.g., due to de-
         Reduction of extracellular osmolarity can  creased perfusion), bradycardia and arterial
       also cause cell swelling, for example, in hypo-  hypertension (through pressure on the brain
       tonic hyperhydration (→ p.122).  stem), squinting (compression of the abducens
         Treatment of prolonged hypernatriemia de-  nerve), and dilated pupils which are unrespon-
       mands caution. The glial cells and neurons  sive to light (compression of the oculomotor
       compensate for the extracellular hyperosmo-  nerve) (→ C2). The pressure gradients bear an
       larity by intracellular accumulation of osmo-  increasing risk of herniation of parts of the
       lytes (e.g., inositol), a process that takes days.  brain  through  the  cerebellar  tentorium
       If the hypernatremia is corrected too quickly,  (→ C3a) or the foramen magnum (→ C3b).
       the osmolytes are not removed quickly enough  The herniated parts compress the brain stem
       and the cells swell.            causing immediate death. If the increase in
         Cerebral edemas of vascular origin occur  CSF pressure is unilateral, the cingulate gyrus
       when there is increased permeability of the  may herniate under the falx cerebri (→ C3),
       cerebral capillaries. The resulting capillary fil-  causing compression of the anterior cerebral
       tration of proteins with osmotically obliged  vessels with corresponding deficits in cerebral
       water (→ B2) thus increases the interstitial  function (→ p. 360).
       space. Among causes of increased permeability
  358  are tumors, infections, abscesses, infarcts,
       bleeding, or poisoning (lead).
       Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
       All rights reserved. Usage subject to terms and conditions of license.
   363   364   365   366   367   368   369   370   371   372   373