J Manipulative Physiol Ther 2000 (Jul); 23 (6): 428–434 ~ FULL TEXT
Benjamin R. Wingfield, BAppSc(Chiro), R. Frank Gorman, MBBS, DO, FRACO
Clovelly Park Chiropractic Clinic,
1230 South Rd,
Clovelly Park, South Australia 5042, Australia
OBJECTIVE: To discuss the case of a patient with severely reduced visual fields arising from terminal glaucomatous retinal damage and the treatment of this condition by spinal manipulation.
CLINICAL FEATURES: A 25–year-old uniocular female patient with congenital glaucoma sought chiropractic treatment for spinal pain, headache, and classic migraine. Advanced optic disk cupping was present, and loss of vision was near complete. A 3–degree island of central vision and a small area of peripheral light sensitivity had remained relatively stable for 3 years after a trabeculectomy procedure that had resulted in intraocular hypotony.
INTERVENTION AND OUTCOME: It was considered possible that chiropractic spinal manipulative therapy may have a positive outcome in visual performance. Before commencing chiropractic spinal manipulative therapy, an ophthalmologic examination was performed, and visual performance was monitored through a course of treatment. Immediately after the first treatment, significant visual field improvement was recorded in the remaining eye. Maximal improvement of vision was achieved after 1 week (4 treatment sessions). Total monocular visual field had increased from approximately 2% to approximately 20% of normal. Corrected central acuity had improved from 6/12 to 6/9. Independent reexamination by the patient's regular ophthalmic surgeon confirmed the results.
CONCLUSION: Recovery of vision in this patient was an unexpected and remarkable outcome, raising the question of whether chiropractic spinal manipulative therapy may be of value in the management of glaucomatous visual field loss. More intensive research is required.
From the Full-Text Article:
Musculoskeletal pathologic features of the cervical spine affecting visual function have generally been ascribed to the function of cervical sympathetic nerves. [4, 5, 8, 23, 25] Barre  proposed that cervical pathology may irritate the sympathetic nerve fibers (termed the “vertebral nerve”) that accompany the vertebral arteries in their course through the foramina transversarium. The resulting sympathetic irritation is presumed to lead to vasoconstriction of the vertebral-basilar arterial system, producing an ischemic condition of the brainstem and occipital lobe (ie, including the visual cortex). This is an attractive theory and has been reiterated by other authors. [5, 25]
Bogduk et al  attempted to assess this theory by electrically stimulating the cervical sympathetics in experimental animals and measuring flow changes in the vertebral and carotid arteries. He found that in regard to flow reduction, “the vertebral artery is only minimally responsive to stimulation of the ‘vertebral nerve’ or the cervical sympathetic trunk.” He did, however, find a pronounced decrease in common carotid arterial flow (to 30% of control). These results are in general agreement with other investigators. [27–31] The lack of significant reduction of blood flow in the vertebral artery led Bogduk to conclude that his results do not support the Barre hypothesis. However, it is questionable how closely the Bogduk methods (and the methods used by the other authors referenced) simulate the effects of mechanical irritation of the vertebral nerve by musculoskeletal pathology. Electrical stimulation of cervical sympathetic nerves at these various locations is not necessarily analogous to mechanical irritation of the vertebral artery and accompanying nerves.
Cervical sympathetic stimulation has been shown to reduce blood supply to the retina in human subjects. Lanigan et al  found that there was a significant difference between the retinal blood flow in the sympathectomized eye and the normal eye of patients with unilateral Horner syndrome while undergoing systemic sympathetic stimulation.
Single photon emission computerized tomography imaging supports the hypothesis of traumatically induced cervical dysfunction leading to reduced blood flow in both the vertebral-basilar system and carotid systems.  Otte et al  found “a characteristic and mostly bilateral hypoperfusion of the parieto-occipital regions of the brain,” thus demonstrating reduced blood flow to both the vertebral area of arterial supply (occipital lobe through posterior cerebral artery) and carotid area of vertebral supply (parietal lobe through middle cerebral artery). Otte et al  have also found this cerebral hypoperfusion to be associated with visual disturbance after cervical spine trauma, with both vision and cerebral perfusion temporarily returning to normal after cervical massage.
As such, we support the notion that subtle cervical musculoskeletal pathologic features may significantly reduce blood flow, at least at the microcirculation level, in the brain stem and cerebrum areas supplied by both the carotid and vertebral-basilar arterial systems.
Expanding on the postulation of subtle cervical musculoskeletal pathologic features resulting in cerebral ischemia, the “cerebral hibernation” theory has been proposed. [23 33, 34]
Neurophysiologic research demonstrates that a fall of blood flow to nervous tissue below a threshold of about 0.1 mL/g per minute results in cell death. [33–34] Another higher threshold has been demonstrated at about 0.17 mL/g per minute. [33–34] Between these thresholds is a state of “ischemic penumbra,” where all electrical activity in the neuron is ceased yet little or no cellular damage occurs. [33–34] On restoration of blood flow, this state is entirely reversible. [33–36] The cerebral hibernation theory proposes that cerebral vasoconstriction produces small, discrete areas of ischemic penumbra at the periphery of capillary beds (ie, these areas are functionally hibernating). As the number of nonfunctional cells increases, so does the disability thus produced so that a greater stimulus is required for patient perception (ie, decreased cerebral sensitivity). We suggest that this may lead to reduction of visual acuity, scotomas, and tunnel vision, with the condition being treatable by spinal manipulation to remove the irritation to the cervical sympathetics.
The notion of neurologic deficits, on occasion being caused by reversible neural hibernation, has clinical support in extracranial to intracranial arterial anastomosis surgery. This procedure has been successful in reversing neurologic deficit after vascular disease by surgical anastomosis of the superficial temporal artery to the intracranial circulation, thus increasing cerebral blood flow. Of particular interest is a report of reversal of long-standing homonymous visual field deficit by this technique. 
In an unusual case such as this one, the question of whether the outcome can be explained by spontaneous remission or by action of placebo must be considered. In this case, spontaneous remission would seem extremely unlikely because improvement of vision was recorded within minutes of the therapeutic intervention, after a period greater than 10 years of visual deterioration, which had been followed by a documented stable baseline of approximately 2 years.
Given the scientific limitations of a case study, the question of placebo can never be fully excluded from such a study. In this case, we believe placebo to be an unlikely explanation for the observations because all parties involved, including the patient, initially had little expectation of a positive visual outcome. In addition, she had undergone numerous surgical procedures and medical interventions throughout her life. Each presumably had at least as great a placebo effect as the current intervention. Had the patient's visual condition been amenable to placebo-induced improvement it would seem reasonable to expect such improvements would have been observed previously.
We believe that there are 2 possible non-placebo—induced explanations of the visual improvement reported in this case study. First, a vascular involvement of the vertebral-basilar arterial system may affect (as previously proposed [11, 14–16, 18–21] in relation to “tunnel vision” functional visual field deficit) cerebral neural function. The patient may have had a functional visual field loss caused by hypoperfusion of the visual cortex, which was superimposed on the glaucomatous visual field loss. As previously described, irritation of the cervical sympathetics and vertebral artery may have produced compromised vertebral-basilar blood flow, resulting in cerebral ischemia and functional hibernation of neurons, which was resolved by chiropractic SMT.
Second, vascular involvement of the carotid system affecting ocular neural function is proposed. An ischemic penumbra effect may have occurred in optic neural tissue, either in the retinal neurons or in the axons of optic nerve head at the site of the optic nerve. The patient's glaucomatous process was no doubt responsible for the ischemic necrosis of ocular neural tissue. However, it is possible that a penumbra of hibernating neurons with marginal blood flow were left between the areas of necrosis and healthy tissue. The state of hibernation may have been maintained by vasoconstriction induced by raised sympathetic tone, which was the result of chronic irritation of the cervical sympathetic nerves by chiropractic subluxation. On appropriate chiropractic SMT and thereby removal of sympathetic irritation, retinal and optic nerve head perfusion was improved, restoring electrical activity in previously hibernating neurons and/or axons.
Because this patient was uniocular, it is impossible to judge from the nature of visual field deficit whether the site of neurologic functional improvement after treatment was anterior to the optic chiasm (and therefore presumably an ocular phenomenon) or posterior to the chiasm (and therefore presumably a cerebral phenomenon). It may be that the visual improvement was a combined function of both processes described above.
Expanding on both hypotheses of a vascular mechanism in this case, we postulate that chiropractic SMT was responsible for the resolution of patient's migraine by a mechanism linked to the improvement of her vision. Chiropractic SMT has been found effective in the treatment of migraine.  It has been shown that the cerebral vasculature of migraine sufferers is generally more irritable (ie, reactive to vasodilatory and vasoconstrictive stimuli) than controls  and that a vasospastic condition is present in migraine sufferers between headaches (“interictal migraine”). [39–41] We believe this interictal migraine to be the condition relieved by chiropractic SMT, which was performed to bring about increased cerebral/ocular blood perfusion. People with migraine have been shown to have a significantly increased incidence of visual field loss than age-matched control subjects, presumably caused by decreased cortical and/or retinal blood perfusion during the interictal period.  Migraine has also been linked to the pathogenesis of glaucomatous optic nerve damage. A statistical link between normal tension glaucoma and migraine has been demonstrated. [43–44] The ability of vasodilative processes to improve visual field deficit caused by glaucomatous damage has been demonstrated in the administration of vasodilators such as nifedipine. [24, 45]
The improvement of this patient's vision after chiropractic SMT suggests a cause-effect relation. We have hypothesized that the presence of chiropractic subluxation in the cervical spine was responsible for irritating the cervical sympathetic nerves, thereby causing the cephalic episodic vascular irritability (ie, migraine) against a background of vascular spasticity (ie, interictal migraine). The resulting compromise of blood supply is thought to produce reduced nervous activity caused by a neural hibernation effect, further reducing visual fields already severely restricted by glaucomatous optic atrophy. Chiropractic SMT was thought to be effective in relieving sympathetic irritation.
It is not known whether this hypothesized vascular phenomenon was of the vertebro-basilar arterial system, thereby affecting vision through reducing neuronal activity of the visual cortex, or of the carotid arterial system, thereby reducing activity of the ocular neural tissue. Should the latter be the case, we postulate that an ischemic penumbra surrounding necrotic optic neural tissue was reversed. This vascular phenomenon may have been present in both arterial systems.
Regardless of the mechanism of the visual improvement, the results of this case study remain remarkable and unexpected, prompting the question whether chiropractic spinal manipulation may be of value in the treatment of glaucomatous field of vision loss.
A need exists for further research, such as blinded, controlled trials of chiropractic SMT in the treatment of visual field loss caused by glaucoma and single photon emission computerized tomography imaging to determine levels of blood flow to the brain and optic structures before and after chiropractic spinal manipulation.
If the results of this case study are reproducible, there are wide implications for the management of glaucomatous visual field loss, especially in normal tension glaucomatous optic atrophy for which no satisfactory treatment is currently available. Other forms of visual field loss may also be amenable to treatment by chiropractic SMT.