Segmental zoster paresis of the left upper limb in a pediatric patient.

Segmental zoster paresis of the left upper limb in a pediatric patient.Segmental zoster paresis is a rare complication of herpes zoster characterized by focal, asymmetrical motor weakness in the myotome that corresponds to the dermatome of the rash. Segmental zoster paresis typically develops within 2-3 wks of cutaneous zoster and predominantly affects the middle-aged and elderly populations. Motor complications rarely develop in children and young adults, but when they do develop, involvement is usually confined to cranial and truncal muscles, with sparing of the limb musculature. A 10-yr-old boy with Fanconi's anemia developed left upper limb weakness because of involvement of C5 motor roots as a complication of herpes zoster. Recognizing motor zoster as a cause of acute motor weakness in a pediatric patient is important in avoiding unnecessary interventions and optimizing treatment.

[Herpetic recurrent upper limb lymphangitis]. / Lymphangite récurrente du membre supérieur d'origine herpétique.

Upper limb lymphangitis often complicates varied wounds on the hand or forearm and improvement is obtained in a few days with adapted antibiotic therapy. A 28-year-old woman presented since few years episodes of lymphangitis of the arm associated with vesicles on an erythematous base, on the palmar face of the first phalanx of the index finger, spontaneous relief within 10 days, without antibiotic therapy. Herpetic origin was confirmed on viral culture. No primary infection neither recurrence was noted. Because of the recurrences, a prophylactic treatment with valaciclovir was instituted. There was no reported recurrence at two years follow-up. Upper limb lymphangitis rarely complicates herpetic whitlow in immunocompetent patient. Clinicians should be aware of viral lymphangitis, which is often overlooked and associated with diagnostic errors and treatment delay.

Segmental zoster paresis of the upper extremity: a case report.

Segmental zoster paresis, a rare complication of herpes zoster, is characterized by focal, asymmetric motor weakness in the myotome that corresponds to the dermatome of the rash. The pathogenesis of segmental zoster paresis is inflammation caused by the spread of the herpes virus. Motor damage may affect the root, plexus, or peripheral nerve. A woman in her early seventies with right shoulder pain and shoulder girdle muscle weakness was diagnosed with involvement of the C5-7 motor roots and upper truncus of the brachial plexus as a complication of herpes zoster. Recognition of herpes zoster as a cause of acute motor weakness is important in avoiding unnecessary interventions as well as in determining the treatment and outcome of the patient. This case is presented to emphasize that herpes zoster infection may be complicated by segmental paresis, which should be considered in the differential diagnosis of acute painful motor weakness of the upper extremity.

Dissociation between titer of anti-ganglioside antibody and severity of symptoms in a case of Guillain-Barré syndrome with treatment-related fluctuation.

Since plasma exchange (PE) and intravenous immunoglobulin (i.v.Ig) have been widely used in treatment for Guillain-Barré syndrome (GBS), early relapse and treatment-related fluctuation have been a potential problem, but little is known about the mechanism of relapse and fluctuation. We describe a patient who had GBS with treatment-related fluctuation. A 37-year-old Japanese man exhibited acute distal-dominant weakness in upper limbs after upper respiratory infection. His cranial nerve system was normal and muscle weakness was limited to upper limbs. Anti-GT1a IgG was strongly positive and anti-GQ1b IgG was also detected in his serum. Muscle weakness responded well to double-filtration plasmapheresis (DFPP) followed by i.v.Ig, but relapsed 45 days after the initial treatment. Although repeated treatments were effective, the patient showed additional minor deterioration twice. Motor nerve conduction velocities (MCVs) corresponded to the muscle weakness, but elevated level of cerebrospinal fluid (CSF) protein remained and anti-ganglioside antibody titers steadily decreased throughout the clinical course. These findings indicate that the clinical fluctuation was not due to changes in the production of anti-ganglioside antibodies but presumably to the transient beneficial effects of DFPP/i.v.Ig and the outlasting inflammatory response in peripheral nerves.