2019 Volume 56 Issue 3 Pages 162-169
The cause of spontaneous cerebrospinal fluid (CSF) hypovolemia is currently considered as CSF leak due to latent spinal injury. Schaltenbrand, the first describer of spontaneous CSF hypovolemia, asserted that the essential cause of CSF hypovolemia was reduced CSF production whether there was CSF leak or not, however. We herein provide a historical review on CSF hypovolemia. Before Schaltenbrand, Hosemann (1909) and Haug (1932) stated that CSF hypovolemia following lumbar puncture was caused by a lack of compensatory CSF production due to underlying autonomic instability, which was corresponding to the current postural tachycardia syndrome (PoTS). Schaltenbrand (1938, 1940) reported 7 cases of spontaneous CSF hypovolemia. Emphasizing the presence of xanthochromia in these cases, he concluded that the cause of spontaneous CSF hypovolemia was reduced CSF production from the choroid plexus, because he had confirmed that so-called CSF was a mixture of liquids produced from the perivascular spaces and from the choroid plexus, and that the former contained larger amount of protein than the latter. Meanwhile, Geller (1940) reported that overwhelming majority cases of CSF hypovolemia accompanied autonomic instability, Recently, Graf et al. (2018) suggested the comorbidity of CSF hypovolemia and PoTS in the same individuals. Sympathetic activity is increased in PoTS patients, while CSF production from the choroid plexus is reported to be under the inhibitory control of the sympathetic nervous system (Lindvall et al., 1978; Haywood et al., 1979). Considering these historical articles together, the essential cause of spontaneous CSF hypovolemia seems to be underlying PoTS.
