Gait ignition failure syndrome, where immobility occurs only upon initiation of ambulation and normal gait ensues once entrained, has been reported with frontal lobe and midbrain locomotor region pathology. However, gait ignition failure syndrome secondary to lumbosacral spinal stenosis has not heretofore been described.

Case Study: A 65-year-old right-handed woman underwent a right frontal parasagittal arteriovenous malformation embolization 25 years prior to presentation. After a fall resulting in a T12 and L1 compression fracture, two kyphoplasties were performed. After the second kyphoplasty, one year prior to presentation, she developed new onset of gait ignition failure, left anterior thigh pain, lower back pain at L5 with radiation to both hips, and bilateral lower extremity weakness. The gait difficulty duration correlates to the duration she is in a seated position. Upon standing, she is unable to move her legs and exhibits basophobia, feeling she may fall due to weakness and she is unable to lift up her left foot to initiate gait, as if it is glued to the floor. She is able to initiate gait after one minute, but has an unsteady scissors-gait for the first few steps. Afterwards, her gaitreturns to baseline. Anteroflexion was noted to eliminate her back and leg pain.

Gait examination shows inability to initiate gait after standing, feeling as if frozen. However, she demonstrated scissors-gait after 30 seconds for 3-5 steps, which gradually improved to baseline. Her quadriceps femoris reflex was absent on the right, 3+ on the left. Her Achilles reflex was absent on left. MRI indicated spinal stenosis with broad based osteophytes at T9-T12 and bilateral neural foraminal stenosis at L1-S1. Exercise therapy designed for spinal stenosis was initiated, and resulted in elimination of gaitignition failure.

Gait ignition failure syndrome may not be necessarily due to frontal or midbrain dysfunction, but can be secondary to lumbosacral impairment. In this patient, dysfunctional arachnoid villi in the lumbosacral nerve roots may have led to transient increases in pressure throughout the neural axis, including the brain, and associated NPH-like symptoms, such as magnetic gait. Seeing that posture affects epidural pressure in lumbar spinal stenosis, with a decrease pressure in response to anteroflexion and reduced pain [Takahashi 1995], one can postulate that this may be a mechanism affecting the patient. Furthermore, since her symptoms are episodic and directly associated with the duration of time she is seated, one may deduce gait ignition failure to be a manifestation of cerebrospinal fluid or intracranial pressure changes influenced by posture. In addition, symptom resolution via exercise therapy strongly suggests that gait apraxia can also be a manifestation of lumbosacral dysfunction. Therefore, those with gait ignitionfailure syndrome warrant evaluation for lumbosacral pathology.

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