IMPROVEMENT OF TICS AFTER SUBTHALAMIC NUCLEUS DEEP BRAIN STIMULATION
Irene Martínez‐Torres, M. I. Hariz, Ludvic U. Zrinzo, Thomas Foltynie, Patricia Dowsey Limousin
Abstract
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Irene Martínez‐Torres, M. I. Hariz, Ludvic U. Zrinzo, Thomas Foltynie, Patricia Dowsey Limousin
Abstract
Open-access reader
Neuropathies that occur in the context of Lyme disease are commonly related to axonal degeneration.1 Acute demyelinating neuropathy has also been described 2 and the possibility of chronic demyelinating neuropathy (CDN) has been raised.3 We report a patient who developed a demyelinating neuropathy in the context of Lyme disease.Treatment of the infection led to marked clinical and electrophysiologic recovery, suggesting an infectious rather than an immune-mediated pathogenesis.Case report.A 56-year-old Caucasian man developed numbness and tingling in his feet in August 2002 that within a few days spread symmetrically to the fingertips and hands.He reported weakness with heavy manual labor over the ensuing 8 weeks.He denied ataxia, cranial nerve, respiratory, or autonomic symptoms.There was no history of diabetes, thyroid disease, or renal disease.There was no exposure to toxins, chemicals, or tick bites.Family history was unremarkable and there was no history of tobacco or alcohol abuse.Cranial nerve examination was normal.Motor examination revealed normal strength in shoulder abduction and elbow flexion bilaterally but strength was Medical Research Council (MRC) grade 4 in elbow extension, wrist extension, and finger extension.In the legs, there was weakness only in bilateral hip flexion (MRC 4).He was globally areflexic with downgoing toes.Sensation to temperature, pinprick, and light touch was reduced up to the knees on both sides.Proprioception was normal but vibratory perception was reduced at the toes and ankles.Coordination, gait, and Romberg test were unremarkable.Complete blood count, serum immunofixation, erythrocyte sedimentation rate, and anti-ENA, GM-1, GD-1b, SGPG, MAG, sulfatide, GALOP, and Hu antibodies were negative.Serum Lyme ELISA, western blot (by Centers for Disease Control and Prevention criteria), and CSF Lyme titer were positive; with ELISA, immunoglobulin G (IgG) titer was 1.2 (positive Ͼ1.09), IgM was negative, and with western blot six IgG bands (18, 39, 41, 58, 66, 93) were seen.CSF revealed one erythrocyte, two From the Department of Neurology, University of Minnesota.
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Neuropathies that occur in the context of Lyme disease are commonly related to axonal degeneration.1 Acute demyelinating neuropathy has also been described 2 and the possibility of chronic demyelinating neuropathy (CDN) has been raised.3 We report a patient who developed a demyelinating neuropathy in the context of Lyme disease.Treatment of the infection led to marked clinical and electrophysiologic recovery, suggesting an infectious rather than an immune-mediated pathogenesis.Case report.A 56-year-old Caucasian man developed numbness and tingling in his feet in August 2002 that within a few days spread symmetrically to the fingertips and hands.He reported weakness with heavy manual labor over the ensuing 8 weeks.He denied ataxia, cranial nerve, respiratory, or autonomic symptoms.There was no history of diabetes, thyroid disease, or renal disease.There was no exposure to toxins, chemicals, or tick bites.Family history was unremarkable and there was no history of tobacco or alcohol abuse.Cranial nerve examination was normal.Motor examination revealed normal strength in shoulder abduction and elbow flexion bilaterally but strength was Medical Research Council (MRC) grade 4 in elbow extension, wrist extension, and finger extension.In the legs, there was weakness only in bilateral hip flexion (MRC 4).He was globally areflexic with downgoing toes.Sensation to temperature, pinprick, and light touch was reduced up to the knees on both sides.Proprioception was normal but vibratory perception was reduced at the toes and ankles.Coordination, gait, and Romberg test were unremarkable.Complete blood count, serum immunofixation, erythrocyte sedimentation rate, and anti-ENA, GM-1, GD-1b, SGPG, MAG, sulfatide, GALOP, and Hu antibodies were negative.Serum Lyme ELISA, western blot (by Centers for Disease Control and Prevention criteria), and CSF Lyme titer were positive; with ELISA, immunoglobulin G (IgG) titer was 1.2 (positive Ͼ1.09), IgM was negative, and with western blot six IgG bands (18, 39, 41, 58, 66, 93) were seen.CSF revealed one erythrocyte, two From the Department of Neurology, University of Minnesota.
Key concepts: Deep brain stimulation, Tics, Subthalamic nucleus, Tourette syndrome, Globus pallidus, Medicine, Movement disorders, Parkinson's disease