Upper Cervical Chiropractic Management of a Patient with Parkinson’s Disease: A Case Report
Erin L. Elster, DC
4880 Riverbend Rd,
Boulder, CO 80301
OBJECTIVE: To discuss the use of upper cervical chiropractic management in managing a single patient with Parkinson’s disease and to describe the clinical picture of the disease.
CLINICAL FEATURES: A 60-year-old man was diagnosed with Parkinson’s disease at age 53 after a twitch developed in his left fifth finger. He later developed rigidity in his left leg, body tremor, slurring of speech, and memory loss among other findings.
INTERVENTION AND OUTCOME: This subject was managed with upper cervical chiropractic care for 9 months. Analysis of precision upper cervical radiographs determined upper cervical mis-alignment. Neurophysiology was monitored with paraspinal digital infrared imaging. This patient was placed on a specially designed knee-chest table for adjustment, which was delivered by hand to the first cervical vertebrae, according to radiographic findings. Evaluation of Parkinson’s symptoms occurred by doctor’s observation, the patient’s subjective description of symptoms, and use of the Unified Parkinson’s Disease Rating Scale. Reevaluations demonstrated a marked improvement in both subjective and objective findings.
CONCLUSION: Upper cervical chiropractic care aided by cervical radiographs and thermal imaging had a successful outcome for a patient with Parkinson’s disease. Further investigation into upper cervical injury as a contributing factor to Parkinson’s disease should be considered.
From the Full-Text Article:
INTRODUCTION
A total of 1.5 million Americans have Parkinson’s disease (PD), more than are afflicted with Multiple Sclerosis and Muscular Dystrophy combined. [1] While PD is generally considered a disease that targets older adults, 15 percent of patients are diagnosed before age 50. [1]
PD, a progressive disorder of the central nervous system, results from destruction of the substantia nigra. The substantia nigra signals the basal ganglia (caudate nucleus and putamen) to secrete dopamine. Because dopamine is an inhibitory neurotransmitter, it is thought that the lack of dopamine allows the basal ganglia to send continuous excitatory signals to the corticospinal motor control system. Therefore, overexcitation of the motor cortex (due to lack of inhibition) creates typical Parkinson’s symptoms such as rigidity (muscle tone increase) and tremors. [1] Current evidence suggests that PD symptoms appear after there has been an 80 percent loss of the dopamine producing cells in the substantia nigra and a similar loss of dopamine synapses with the basal ganglia. [1]
Diagnosis of PD occurs through patient history and neurological exam and is best determined by a physician specializing in movement disorders. No definitive laboratory test exists to diagnose or predict PD.
PD symptoms often begin with an episodic tremor of the hand on one side of the body. Over time, resting tremors can be accompanied by slowness, stiffness, and lack of arm swing on the affected side. As symptoms progress, impairment may extend to the other side of the body. Because of fine motor deficits, finger and hand movements requiring skilled coordination, such as brushing teeth, buttoning clothes, and handwriting may become slow and difficult. Patients may notice a foot drag on the affected side, a slowed gait, shorter steps, or freezing (inability to start) when initiating movement. Voices may lose volume and facial expressions may become masked.
The standard medical treatment for PD has been the administration of a combination of levodopa (a short-acting drug that enters the brain and is converted into dopamine) and carbidopa (enhances levodopa’s action in the brain). Several neurosurgical techniques also exist, including thalamotomy (destruction of ventral thalamus to control tremor), pallidotomy (destruction of posterior ventral globus pallidus to control hyperkinetic symptoms), and deep brain stimulation (electrode implantation for patient-controlled stimulation of thalamus to control tremor). [1] Although the medications and surgeries may temporarily control symptoms, they neither stop nor reverse the progressive degeneration of the substantia nigra.
Palmer reported treatment of PD patients with upper cervical chiropractic care as early as 1934. [2] In his writings, he referred to patients with “shaking palsy” and listed improvement or correction of symptoms such as “tremor, shaking, muscle cramps, muscle contracture, joint stiffness, fatigue, incoordination, trouble walking, numbness, pain, inability to walk, and muscle weakness.” His treatment included paraspinal thermal scanning using a neurocalometer (NCM), a cervical radiographic series to analyze the upper cervical spine, and a specific upper cervical adjustment performed by hand on a knee-chest table.
No other reference for the chiropractic management of PD was found. To the author’s knowledge, this is the first report on this topic in recent decades.
Discussion
An important aspect of this patient’s medical history was his recollection of head and/or neck traumas before the onset of PD. He recalled 6 specific incidences of trauma preceding the onset of symptoms, including 2 concussions while playing football, twice hitting his head against a windshield (during a helicopter crash and an auto accident), a sledding accident in which his legs were paralyzed for 24 hours, and a riding accident in which he was thrown from a horse. The body of medical literature detailing a possible trauma-induced cause for PD, or at least a contribution, is substantial. [26-31] In fact, medical research has established a connection between spinal trauma and numerous neurologic conditions besides PD, including but not limited to multiple sclerosis, epilepsy, migraine headaches, vertigo, amyotrophic lateral sclerosis, and attention deficit/hyperactivity disorder. [32-38] Although medical research shows that trauma may lead to PD and the other neurologic conditions mentioned above, no mechanism has been defined. I hypothesize that the missing link may be the injury to the upper cervical spine.
Although various theories have been proposed to explain the effects of chiropractic adjustments, a combination of 2 theories seems most likely to explain the profound changes seen in this patient with PD after he received upper cervical chiropractic care. The first mechanism, central nervous system facilitation, can occur from an increase in afferent signals to the spinal cord and/or brain coming from articular mechanoreceptors after a spinal injury. [39-43] The upper cervical spine is uniquely suited to this condition because it possesses inherently poor biomechanic stability along with the greatest concentration of spinal mechanoreceptors.
Hyperafferent activation (through central nervous system facilitation) of the sympathetic vasomotor center in the brainstem and/or the superior cervical ganglion may lead to the second mechanism, cerebral penumbra, or brain hibernation. [44-50] According to this theory, a neuron can exist in a state of hibernation when a certain threshold of ischemia is reached. This ischemia level (not severe enough to cause cell death) allows the cell to remain alive, but the cell ceases to perform its designated purpose. The brain cell may remain in a hibernation state indefinitely, with the potential to resume function if normal blood flow is restored. If the degree of ischemia increases, the number of functioning cerebral cells decreases and the disability worsens.
It is likely that this patient sustained an injury to his upper cervical spine (visualized on cervical radiographs) during one or more of the traumas he experienced. It is also likely that because of the injury, through the mechanisms described previously, sympathetic malfunction occurred (measured by paraspinal digital infrared imaging), possibly causing a decrease in cerebral blood flow. If blood supply to this patient’s substantial nigra was compromised, it is possible that a certain percentage of those cells were existing in a state of hibernation rather than cell death. Therefore the combination of theories suggests that when blood supply was restored to the hibernating substantial nigra cells (from upper cervical chiropractic care), the cells resumed their dopaminergic (dopamine-secreting nerve fibers) function. However, few conclusions can be drawn from a single case. Indeed, this patient was treated with upper cervical chiropractic along with 9 other patients with PD during a 3-month period. Therefore further research is recommended to study the links among trauma, the upper cervical spine, and neurologic disease.
Conclusion
This case report described a successful outcome for a patient with PD who was treated with upper cervical chiropractic care. To my knowledge, this is the first case reported on this topic since Palmer’s research 70 years ago.2 No firm conclusion can be obtained from the results of one case, although these results do suggest that upper cervical chiropractic care may provide benefit for patients with PD when an upper cervical injury is found. Further investigation into upper cervical injury and resulting neuropathophysiology as a possible cause or contributing factor to PD should be considered.
