Medical doctor since 1972. The rash features raised dots that eventually turn into blisters. Likely due to American television advertisements, the shingles vaccine has been the topic of discussion. RLS affects 5–10% of the general population, and it may be a primary (idiopathic) or secondary disorder. Secondary types are mainly associated with iron deficiency, uraemia, pregnancy, neuropathy and myelopathy. He had history of two attacks of herpes zoster at the same site for 5 years and complete recovery with antiviral agent. Oxygen based colon cleansers other digestive aids such as probiotics and digestive enzymes are also available from good specialist manufacturers.
He also reports extreme stress at work with many deadlines and an ongoing threat of job loss because of continuing downsizing due to overseas corporate operations. He completed a Pharmacy Practice Residency at the University of Arizona/University Medical Center in 1996. A dose of 0.25 mg/day of ropinirole has clearly improved his symptoms.4 Neurological examination showed no clues pointing to a secondary form of RLS. The day before presentation, he had experienced sudden and severe neck pain, which radiated to both the shoulders. The pain decreased in the supine position and re-emerged in the upright position. It was accompanied by a weakness of his proximal shoulder muscles with a feeling of ‘light-headedness’. The vaccine is recommended for the prevention of herpes zoster and its complications in persons 60 years and older without contra-indications.
He recognised this leg sensation as the same as his RLS leg sensation; however, it was much worse than he had ever experienced before. The patient decided to go to the emergency room (ER) when this acute and very disturbing exacerbation of his already established RLS started. There was no percussion tenderness in lower back and left buttock. Taking of prednisone and immuno globulin are also part of the treatment. Focal reactivation along the ganglial distribution in adulthood leads to herpes zoster. There was a decreased sense of pain in the C4–C6 dermatomes, but touch and vibration senses were normal. Muscle strength and tonus in his arms and legs were normal, but his gait was spastic and his tendon reflexes were normal with bilateral extensor plantar responses.
Bladder catheterisation showed 1 litre urinary retention. A cervical spinal cord lesion was suspected. MRI study of the cervical spine revealed signal hyperintensities on T2-weighted images and diffusion-weighted images, with reduced signal intensity on the apparent diffusion coefficient images (ADC) at the centre of the C3–C6 levels of the spinal cord (A,B). A diagnosis of cervical spinal cord infarction was made. In order to identify the cause of stroke, extensive diagnostic work was done. Laboratory testing and cerebrospinal fluid examination showed no abnormalities. Straight leg raise test was not able to do due to severe back pain.
(A) Axial MRI of T2-weighted images made 36 h after symptom onset showing increased signal in the spinal cord at level C3–C6. Involvement of the geniculate ganglion can produce Ramsay Hunt syndrome or herpes zoster oticus. Four months later, he still experienced constipation and difficulty with voiding (a delayed urge). His gait was normal and there were no signs of orthostatic hypotension. With the application of the rotigotine transdermal patch (2 mg) and 0.25 mg a day of ropinirole, the patient no longer experienced the urge to move. The exact pathophysiology of RLS is uncertain. However, RLS is a network disorder.
Many regions of the nervous system contain structures that are involved in somatosensory perception and the generation of movement.1 This diversity makes it reasonable to assume that changes in different parts of the nervous system may cause RLS. Currently, it is unclear as to whether RLS originates from the cortical, subcortical or in the spinal cord. Several experimental animal studies as well as case reports of patients who developed RLS in association with spinal cord lesions have given rise to the hypothesis that interruption of the spinal pathways is a part of the aetiology of RLS.2356 However, the exact role of the spinal cord in the origination of RLS is not yet completely understood. This figure shows the sagittal and axial magnetic resonance images of the thoracolumbar spine. It has been suggested that A11 neurons play a central role. The mainstays of treatment are antiviral therapy and analgesia. The A11 neurons project to the sensory dorsal horn and the intermediolateral nucleus (IML).
The dopaminergic projections of the A11 on the IML exert direct inhibitory actions on sympathetic preganglionics. Thus, an impairment of the A11 inhibitory function would shift the balance of descending control of the sympathetic preganglionics towards excitation. This leads to the activation of high threshold muscle afferents and focal akathisia. In an animal experimentation study, A11-lesioned mice showed increased locomotor activity in a dark room.7 The cervical spinal cord ischaemia in our patient possibly interfered with the descending A11 dopamine pathway to the spinal cord and may thus have caused the RLS exacerbation and the autonomic dysfunction in our patient. According to the 2012 European guidelines on the management of RLS, dopaminergic agents are the first-line treatment for primary RLS. Although their working mechanisms are not fully clarified as yet, it is assumed that dopaminergic agents stimulate D2-like (D2, D3 and D4) receptors. This stimulation, just like endogenous dopamine, exerts direct inhibitory actions on sympathetic preganglionics and inhibitory control over the ascending nociceptive input.
Herpes zoster is diagnosed clinically by a prodrome of 1-3 days, unilateral pain, grouped vesicules, and rash history in the same distribution. Our case supports the hypothesis that interruption of the spinal cord pathways are part of the aetiology of RLS. Further research is needed to unravel the complex RLS pathophysiology. The dopaminergic projections of A11 on the intermediolateral nucleus exert direct inhibitory actions on sympathetic preganglionics, and impairment of the A11 inhibitory function shifts the balance of descending control of the sympathetic preganglionics towards excitation.