Deroy C, Bismuth C, Chuzel T, Watrelot-Virieux D, Carozzo C and Escriou C
A 10 year old Chow Chow presented with a 24 hour history of acute signs of spastic paraparesis following an 11 months history of progressive pelvic limb ataxia. CT myelography revealed several chronic disk protrusions. Twelve hours after lumbar puncture, the dog displayed signs of multifocal central nervous system lesions (spastic tetraplegia, head tilt, nystagmus, amaurosis, myosis, altered consciousness, ataxic breathing pattern). Magnetic resonance imaging of the brain was abnormal. On cisternal tap, bloody cerebro spinal fluid (CSF) "spurted" (elevated opening pressure) and had signs of recent hemorrhage (xanthochromia, no platelets). The dog was euthanized 48 hours post CT. At necropsy, diffuse, massive SAH was observed throughout spinal cord, brain stem, cerebellum and forebrain with no signs of hemorrhage at any other location. Histopathology confirmed subarachnoid location of the hemorrhage. The most commonly proposed pathophysiologic mechanism for subarachnoid hemorrhage following lumbar puncture is persistent CSF leakage at the puncture site resulting in CSF volume depletion and traction/ rupture of subdural bridging veins. Alternative pathophysiologic mechanisms include traumatic lumbar puncture and anticoagulant effect of non-ionic contrast agent. Brain dysfunction is thought to be the consequence of brain ischemia. Although extremely rare, this life threatening condition must be included as a possible complication of lumbar myelography or CT myelography.
