Urban Chiropractic

The Effects of Chiropractic Spinal Adjustments in a Case of Uveitis

Anterior uveitis refers to an inflammatory condition of the iris and ciliary body, while posterior uveitis refers to an inflammatory condition of the choroid.¹ Both conditions cause blurred vision due to opacities in the intraocular fluid. In addition, lesions within the eye cause reduced vision and increased awareness of floaters, dark spots that drift across the field of vision.¹ Children with uveitis may report pain, photophobia, lacrimation, blepharospasm, and disturbed vision – or, the patient may be asymptomatic. Several researchers report correlations between uveitis and other conditions, such as ankylosing spondylitis, sacroilitis, juvenile chronic arthritis, herpes simplex and connective tissue diseases.²Other studies show a correlation between posterior uveitis and disorders of the central nervous system, such as toxoplasmosis. However, one third of patients with uveitis display no association with any other diseases.^2,3

In a case study, a male child aged 5.75 years was diagnosed with anterior and posterior uveitis based on a thorough ophthalmological examination. Visual acuity was 20/100 in the right eye and 20/30 in the left eye; slit lamp examination showed evidence of anterior uveitis with 2+ cells and flare in each anterior chamber; and a broken synechia was identified in the right eye with mild changes of the lens consistent with inflammation.¹ Ophthalmoscopic monitoring continued over a four month course of topical and systemic steroid therapy. However, no significant improvement was observed based on the Snellen eye chart and fundus examination. Therefore, steroid therapy was discontinued and chiropractic treatment was taken into consideration.¹

During the chiropractic consultation, a thorough history was performed. The patient suffered from chronic bronchitis since infancy; at three years, the patient fell from the bed and lacerated his left eyelid; at five years, the patient fell from the bed again and reported leg and knee pain; the patient complained of intermittent neck and back pain and leg, knee, and ankle pain; and lastly the patient complained of pain in the proximal interphalangeal joints of all fingers.² During spinal examination, the patient presented with a mild dextro-scoliosis in the thoracic spine and a mild levoscoliosis in the lumbar spine. Although the range of motion in the cervical spine was normal, pain at C3 to C5 was noted during neck extension.² Furthermore, the patient reported pain at C7 during forward flexion, and pain in the area of the contralateral trapezius muscle during neck rotation.² Lastly, static and motion palpation of the spine revealed segmental subluxations, muscle induration, fixation, and misalignments at several spinal levels.¹ Therefore, a course of spinal adjustments was commenced.

Spinal adjustments were initially delivered at a frequency of three times per week and later reduced to two times per month after improvement in visual acuity was achieved. After the second visit for spinal adjustment, visual acuity was 20/80 in the right eye and 20/20 in the left eye. After the sixth visit, visual acuity was 20/50 in the right eye and 20/20 in the left eye. A year after chiropractic treatment, an ophthalmologist and optometrist verified improvement in visual acuity (20/30 for the right eye) based on Snellen chart tests.¹

To understand the link between uveitis and spinal adjustment therapy, one must consider the neurological and internal anatomy of the eye. The superior cervical ganglion receives preganglionic fibers from the first thoracic nerve and supplies postganglionic fibers to the internal carotid and cavernous plexuses. In turn, the internal carotid and cavernous plexuses supply sympathetic fibers to the vasculature of the eye. Alteration of the sympathetic nerve supply may lead to tissue neovascularization and increase the possibility of rupture with trauma and histamine release.⁴Therefore, correction of associated nerve irritation via spinal adjustment may reverse symptoms of uveitis.

References

1) Manuele, J and Fysh, P. “The Effects of Chiropractic Spinal Adjustments in a Case of Bilateral Anterior and Posterior Uveitis.” Journ of Clin Chiro Ped. 2004; 6:334-337.

2) Szanto E, Granfors K, Wretlind B. Acute anterior uveitis, arthritis and enteric antigens. Clin Rheumatol 1991; 4:395-400.

3) Linssen A, et al. “The lifetime cumulative incidence of acute anterior uveitis in a normal population and its relation to ankylosing spondylitis and histocompatibility antigen HLAB27.” Ophthal Vis Sci. 1991; 9:2568-78.

4) Oski, FA. Principles and Practice of Pediatrics, 2nd ed. Philadelphia; Lippincott 1994; 34:891.

Sciatica: Symptoms, Mechanisms, and Treatment

Sciatica is a debilitating condition in which patients experience pain or paresthesia along the path of the sciatic nerve in a dermatomal pattern. Up to 2 cm in diameter, the sciatic nerve is the largest in the body and – directly or indirectly – innervates the hamstrings, lower extremity adductors, calf muscles, anterior lower leg muscles, and intrinsic foot muscles.^1-3 In the general population, the annual prevalence of disc related sciatica is 2.2%.¹ In patients with low back pain, the annual prevalence is 5-10%.¹ Risk factors include age, height, smoking, stress, strenuous activity, and exposure to whole body vibration (e.g. in a car).⁴ Epidemiologically, sciatica displays no gender predominance, peak incidence in the fourth decade, a genetic predisposition, and an occupational predisposition (e.g. in machine operators and truck drivers).⁴

Sciatica is primarily diagnosed by history taking and physical examination. Patients with sciatica commonly report unilateral pain in the lumbar spine, pain or burning sensations deep in the buttocks, and paresthesia.⁵ Less commonly, patients report ipsilateral leg weakness. Physical examination depends on neurological testing, such as the straight leg raising test. In the straight leg raising test, the patient lays in a relaxed, supine position while the examiner lifts the leg from the posterior, flexing at the hip joint and keeping the knee in full extension. Typically, pain experienced between 30 and 70 degrees of hip flexion indicates a lumbar disc herniation.⁴ Overall, the diagnosis of sciatica is justified if a patient reports radiating pain in one leg and demonstrates nerve root tension or neurological deficits based on a positive result on one or more neurological tests.⁴

Anatomically, the sciatic nerve is comprised of the L4 through S2 nerve roots, which merge at the pelvic cavity and exit posteriorly through the sciatic foramen.⁵ The sciatic nerve then travels inferior and anterior to the piriformis, and posterior to the gemellus superior, gemellus inferior, obturator internus, and quadratus femoris.⁵ Next, the sciatic nerve enters the posterior thigh, travels to the biceps femoris, and terminates at the knee in the popliteal folsa.⁵ Sciatica occurs when the nerve is pinched or compressed anywhere along the aforementioned pathway. In 90% of cases, sciatica is caused by a herniated disc with associated nerve root compression.⁴ However, sciatica is also caused by several other pathologies, including:

Muscle spasm

Nerve root impingement

Epidural abscess

Epidural hematoma

Tumor

Spinal tuberculosis

Piriformis syndrome

The prognosis for sciatica is quite favorable, with most cases resolving in 4 to 6 weeks with no long-term consequences. For example, a randomized trial involving non-steroidal anti-inflammatory drugs showed that 60% of patients recovered within three months and 70% within 12 months.⁶ That said, recovery is more prolonged in severe cases involving neurological deficits. Accordingly, some studies suggest that up to 30% of patients experience pain for a year or longer.^6-7 Therefore, it is advised to seek treatment to avoid chronic and recurrent pain.

Chiropractic treatment for sciatica is non-invasive, non-surgical, and drug-free. The type of treatment depends on the cause of sciatica, but may include a combination of ice therapy, ultrasound, transcutaneous electrical nerve stimulation, and spinal adjustments. Ice therapy alleviates sciatic pain by reducing inflammation.⁸ Ultrasound therapy involves sound waves that penetrate deep into soft tissue, which increases circulation and reduces muscles spasms, cramping, swelling, stiffness, and sciatic pain.⁸

In transcutaneous electrical nerve stimulation, a machine generates variable amounts of electrical current to reduce muscle spasms and alleviate pain.⁸ Spinal manipulation frees restricted movement of the spine by restoring misaligned vertebral bodies to their proper position in the spinal column; this alleviates inflammation, muscle spasms, and sciatic pain.⁸ Overall, sciatica is a debilitating condition that can significantly affect one’s quality of life. Patients displaying symptoms should seek chiropractic care to alleviate their pain and restore their quality of life.

References

1) Lagerbäck T, Fritzell P, Hägg O, Nordvall D, Lønne G, Solberg TK, Andersen MØ, Eiskjær S, Gehrchen M, Jacobs WC, van Hooff ML, Gerdhem P. Effectiveness of surgery for sciatica with disc herniation is not substantially affected by differences in surgical incidences among three countries: results from the Danish, Swedish and Norwegian spine registries. Eur Spine J. 2019 Nov;28(11):2562-2571.

2) Alrwaily M, Almutiri M, Schneider M. Assessment of variability in traction interventions for patients with low back pain: a systematic review. Chiropr Man Therap. 2018;26:35.

3) Hong X, Shi R, Wang YT, Liu L, Bao JP, Wu XT. Lumbar disc herniation treated by microendoscopic discectomy : Prognostic predictors of long-term postoperative outcome. Orthopade. 2018 Dec;47(12):993-1002.

4) Koes BW, van Tulder MW, Peul WC. Diagnosis and treatment of sciatica. BMJ. 2007;334(7607):1313–1317.

5) Delgado-López PD, Rodríguez-Salazar A, Martín-Alonso J, Martín-Velasco V. [Lumbar disc herniation: Natural history, role of physical examination, timing of surgery, treatment options and conflicts of interests]. Neurocirugia (Astur). 2017 May – Jun;28(3):124-134.

6) Weber H, Holme I, Amlie E. The natural course of acute sciatica with nerve root symptoms in a double blind placebo-controlled trial of evaluating the effect of piroxicam (NSAID). Spine 1993;18:1433-8.

7) Vroomen PCAJ, Krom MCTFM de, Slofstra PD, Knottnerus JA. Conservative treatment of sciatica: a systematic review. J Spinal Dis 2000;13:463-9.

8) Grassi R. Chiropractic Treatment of Sciatica. Remedy Health Media. Spine Universe. 2020.

Migraines: Presentation, Mechanisms, and Management

Migraines remain an important public health issue that can significantly affect one’s daily activities and quality of life. The prevalence of migraines in the US adult population is quite high, affecting 15.3% of individuals. Relative to the general population, the prevalence is higher for those with disabilities (16.4%), aged 18-44 (17.9%), and on low income (19.9%). Additionally, the prevalence in women (20.7%) is much higher than in men (9.7%). Annually, migraines account for 3% of all visits to the emergency department, consistently among the top four or five leading causes.¹

Symptomatically, migraines progress through four stages: prodrome, aura, attack, and post-drome. One to two days before a migraine – i.e. prodrome – subtle changes warn of an upcoming attack, including constipation, mood changes, food cravings, neck stiffness, increased thirst, and frequent yawning. As a migraine progresses, individuals may experience auras, or reversible symptoms of the nervous system that begin gradually and last 20 to 60 minutes. Examples of auras include visual phenomena (e.g. bright spots, shapes, and flashes), vision loss, pins and needles in the arms and legs, facial numbness, difficulty speaking, hearing noises, and uncontrollable jerking movements. During an attack, which can last 4 to 72 hours if untreated, individuals may experience pain on one or both sides of the head, throbbing sensations, sensitivity to light and sound, nausea, and vomiting. After an attack – i.e. post-drome – individuals may feel drained and confused for up to a day.²

Over the past few decades, our understanding of the pathophysiology of migraines has improved considerably. Previously, the vascular theory was the leading explanation for migraines; however, a series of imaging studies demonstrated that vascular changes were neither necessary nor sufficient for attacks.^3-4 From vascular theories, researchers moved to neuronal theories involving the peripheral and central nervous systems. Initially, researchers attempted to localize a single structure as the source of migraines; but it is now clear that migraines are a complex brain network disorder with a genetic basis that involves multiple cortical, subcortical, and brainstem regions.^4-6

The trigeminovascular system is a key actor and its activation is thought to initiate the cascade of events resulting in migraines due to its direct connection with the diencephalic and brainstem nuclei.^7-8 The literature also supports the involvement of the hypothalamus in migraines. For example,several studies demonstrate hypothalamic connections to the thalamus, trigeminovascular system, and brainstem nuclei, supporting the role of the hypothalamus in pain modulation in patients with migraines.^9-11 The involvement of the hypothalamus may explain some of the early symptoms of migraines, such as food cravings, mood swings, and yawning. Additionally, the thalamus may play a role in migraines. The thalamus is a nociceptive relay station that conveys information from the dura mater and cutaneous areas to second-order trigeminovascular areas. Several studies report structural and functional thalamic alterations in patients with migraines.^12-13 Furthermore, changes in the structure and function of key cortical areas were demonstrated in migraineurs, such as the insular, somatosensory, prefrontal, and cingulate cortex.¹⁴ Lastly, a variety of factors may trigger migraines, including hormonal changes in women, alcohol, coffee, stress, sensory stimuli, sleep changes, weather changes, medication, and processed foods.

Chiropractic spinal manipulative therapy (CSMT) is supported by numerous studies as an effective treatment option for migraines. In a randomized controlled trial of 172 patients, Tuchin et al demonstrated that patients receiving CSMT reported a significant improvement in migraine frequency, duration, disability, and medication use. A more recent study by Chaibi et al involved a 52 year old woman suffering from migraines once per month, with pain scored as an 8 out of 10. After CSMT treatment, the patient reported a complete elimination of migraines. At a follow up 6 months later, the patient did not report a single migraine episode during the intervening period.¹⁶ Overall, evidence suggests that CSMT can alleviate pain from migraines, making chiropractic care a viable option for individuals suffering from migraines.

References

1) Burch R, Rizzoli P, Loder E. The prevalence and impact of migraine and severe headache in the United States: figures and trends from government health studies. Headache: The Journal of Head and Face Pain. 2018;58(4):496–505.

2) Mayo Clinic Staff. Migraine. Mayo Foundation for Medical Education and Research. Nov. 2019.

3) Amin FM, Asghar MS, Hougaard A, Hansen AE, Larsen VA, de Koning PJ, Larsson HB, Olesen J, Ashina M. Magnetic resonance angiography of intracranial and extracranial arteries in patients with spontaneous migraine without aura: a cross-sectional study. Lancet Neurol. 2013;12:454–461.

4) Goadsby PJ, Holland PR, Martins-Oliveira M, Hoffmann J, Schankin C, Akerman S. Pathophysiology of migraine—a disorder of sensory processing. Physiol Rev. 2017;97(2):553–622.

5) Charles A. Migraine: a brain state. Curr Opin Neurol. 2013;26:235–239.

6) Ferrari MD, Klever RR, Terwindt GM, Ayata C, van den Maagdenberg AM. Migraine pathophysiology: lessons from mouse models and human genetics. Lancet Neurol. 2015;14:65–80.

7) Goadsby PJ, Charbit AR, Andreou AP, Akerman S, Holland PR. Neurobiology of migraine. Neuroscience. 2009;161:327–341.

8) Akerman S, Holland PR, Goadsby PJ. Diencephalic and brainstem mechanisms in migraine. Nat Rev Neurosci. 2011;12:570–584.

9) Kagan R, Kainz V, Burstein R, Noseda R. Hypothalamic and basal ganglia projections to the posterior thalamus: possible role in modulation of migraine headache and photophobia. Neuroscience. 2013;248:359–368.

10) Abdallah K, Artola A, Monconduit L, Dallel R, Luccarini P. Bilateral descending hypothalamic projections to the spinal trigeminal nucleus caudalis in rats. PLoS One. 2013;8:e73022.

11) Robert C, Bourgeais L, Arreto CD, Condes-Lara M, Noseda R, Jay T, Villanueva L. Paraventricular hypothalamic regulation of trigeminovascular mechanisms involved in headaches. J Neurosci. 2013;33:8827–8840.

12) Magon S, May A, Stankewitz A, Goadsby PJ, Tso AR, Ashina M, Amin FM, Seifert CL, Chakravarty MM, Muller J, Sprenger T. Morphological abnormalities of thalamic subnuclei in migraine: a multicenter MRI study at 3 tesla. J Neurosci. 2015;35:13800–13806.

13) Hodkinson DJ, Wilcox SL, Veggeberg R, Noseda R, Burstein R, Borsook D, Becerra L. Increased amplitude of thalamocortical low-frequency oscillations in patients with migraine. J Neurosci. 2016;36:8026–8036.

14) Sprenger T, Borsook D. Migraine changes the brain: neuroimaging makes its mark. Curr Opin Neurol. 2012;25:252–262.

15) Tuchin P, Pollard H, Bonello R. A randomized controlled trial of chiropractic spinal manipulative therapy for migrain. J Manip Physio Therap. 2000;23:91-95.

16) Chaibi A, Tuchin PJ. Chiropractic spinal manipulative treatment of migraine headache of 40-year duration using Gonstead method: a case study. J Chiropr Med. 2011;10(3):189–193.