One patient patient 12 had involvement of cranial nerves, with hearing impairment, diplopia and left ptosis. One patient patient 13 had associated sensory ataxia. Six patients had systemic illness. Four patients had MM initially, but as the condition worsened, it became less multifocal and more symmetrical. The most prominent finding was the high incidence of vasculitic neuropathy, which affected six patients.
In this subgroup, necrotizing arteritis was demonstrated in two patients; one had a type 1 vasculitic lesion and the other had a type 2 vasculitic lesion. Histological signs of necrotizing arteritis type 1 included segmental necrosis of the wall of epineurial and perineurial arteries, transmural inflammatory cell infiltration and occlusion of the lumen. Wallerian degeneration affected the majority of nerve fibers simultaneously, and larger myelinated fibers were more prone to axon loss Figure 1.
Histological signs of type 2 vasculitis included necrotizing arteritis, but without transmural inflammatory cell infiltration. Pathological diagnosis confirmed type 3 vasculitic lesion. Pathological typing of vasculitic lesions is detailed in the literature Oh, The walls of two perineurial arteries showed signs of necrosis, transmural inflammatory cell infiltration and occlusion of the lumen.
Of the six cases with vasculitic neuropathy, three patients patients 1, 2 and 6 had systemic vasculitis i. The mean interval between the onset of symptoms and referral for biopsy was 40 months range: 24—60 months. Three patients had MM as the pattern of nerve injury at onset. Two of these patients patients 1 and 2 became less multifocal and more symmetrical, characteristic of ASMN, over time 2 months and 6 months later, respectively. The other patient patient 6 continued to have MM as the pattern of nerve injury over a period of 36 months. Electrophysiological investigation in this subgroup showed that two patients patients 1 and 6 had axonal ASMN and one patient patient 2 only had mononeuropathy.
This highlights the inconsistency between the clinical features and electrophysiological characteristics; the electrophysiological abnormalities were asymmetrical in all three patients. Three patients patients 3, 4 and 5 had nonsystemic vasculitic neuropathy NSVN. The mean interval between the onset of symptoms and referral for biopsy was Two patients patients 3 and 4 had mononeuropathy as the pattern of nerve injury at onset, but progressed to MM over time 1 month and 0.
Electrophysiological investigation was normal in patient 3, but pathology of the sural nerve was abnormal and showed inflammatory infiltrates in the vicinity of nerve vessels associated with mild axonal degeneration of nerve fibers. This finding indicates that pathological changes might precede electrophysiological changes Figure 2. Two patients patients 9 and 10 were diagnosed with NSVN based on clinical, laboratory and electrophysiological findings. The nerve biopsies did not contribute to the diagnoses.
Patients 7 and 8 had suspected NSVN based on clinical and electrophysiological findings. The pathological findings of sural nerve biopsy were consistent with perineuritis. The sural nerves of two patients patients 7 and 8 demonstrated multifocal perineurial inflammation consisting mostly of mononuclear lymphocytes accompanied by histiocytes and perineurium thickened by collagen. This response was limited to the perineurium and did not involve the endoneurium Figure 3. There was no evidence of necrotic vasculitis. Affected fascicles showed prominent axon loss, while others displayed axonal degeneration.
Uninflamed fascicles showed mild axon loss. HLA-positive cells had infiltrated all fascicles, and had generally infiltrated the perineurium. Electron microscopy showed that the basement membrane of perineurial cells was thickened, that perineurial collagen was increased, and that perineurial cells had undergone degeneration. Patient 7 showed perivascular lymphocyte infiltration, and patient 8 had no vascular changes.
These two patients were thus diagnosed with perineuritis based on pathological characteristics. Both patients were improved with methylprednisone and immune inhibitors. Sural nerve fascicle showed a thickened perineurium with infiltration of mononuclear cells. The two patients had mononeuritis multiplex. Both had initial symptoms of numbness and pain, and then sensory and motor involvement. The mean interval between the onset of symptoms and referral for biopsy was 2.
Neither of our patients had raised CSF protein. Electrophysiological investigation showed that compound motor action potentials CMAPs were remarkably reduced in several motor nerves. Sensory nerve conduction velocity of all examined nerves was normal in both patients. Patient 7 had a swollen lymph node with good activity. B-mode ultrasonography showed a lymph node diameter of less than 1 cm with clear structure. Patient 8 had a past history of oral ulcer, but did not fit the criteria for diagnosis of Behcet's disease.
Three patients patients 11, 12 and 13 suffered from a chronic inflammatory demyelinating polyradiculoneuropathy CIDP based on clinical features and laboratory data. The mean interval between the first symptoms and the biopsy was 4 months range: 3—5 months. All three patients in this subgroup had MM as the pattern of nerve injury at onset. Two of these patients patients 11 and 13 developed ASMN over time 2 months and 0.
Patient 12 had involvement of the cranial nerves, and patient 13 had associated sensory ataxia. All improved by intravenous administration of methylprednisone. Electrophysiological investigation in patients 12 and 13 showed multifocal demyelination. There was slight perineurial macrophage infiltration in patient In summary, these two patients were diagnosed with CIDP based on clinical features, laboratory data and electrophysiological characteristics.
The nerve biopsies confirmed the clinical diagnoses. Electrophysiological study of patient 11 showed that sensory nerve action potentials SNAPs were remarkably reduced in the right ulnar nerve and right sural nerve.
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CMAPs and motor nerve conduction velocity of all examined nerves were normal. Nerve biopsy showed mild demyelination. Therefore, patient 11 was diagnosed with CIDP based on clinical features and laboratory data, although the electrophysiological characteristics and nerve biopsy could not confirm the clinical diagnosis. Patient 14 was diagnosed with Lewis-Sumner syndrome, i. Patient 14 was a young man with initial symptoms of sensory and motor deficit in the bilateral ulnar nerves.
After intravenous injection of immunoglobulins, symptoms soon improved, although there was still slight weakness in the right ulnar of two fingers. Six months later, he had numbness and pain in the left ulnar of two fingers and weakness in his right foot. The CSF was normal. Electrophysiology showed multifocal demyelination associated with conduction block in nonentrapment sites in the bilateral ulnar nerves. Mild demyelination was found on nerve biopsy Figure 5. Genetic studies did not identify chromosome 17 mutations.
Skin biopsy was performed in 8 cases patients 1, 2, 4, 5, 7—10 clinically suspected with vasculitic neuropathy. The presence of inflammatory infiltrates in the vicinity of dermis vessels was found in 3 patients patients 1, 5 and 7 , but no necrotizing arteritis was observed.
There were no significant changes in skin biopsy among the other five patients. In this study, skin biopsy did not contribute to the final diagnoses. MM is an unusual form of peripheral neuropathy. Its global incidence is unknown because of the wide variety of underlying pathologies that may lead to the disorder. MM is actually a group of disorders, not a true distinct disease entity, and may be seen in association with a variety of systemic illnesses, as we report here. Our 14 patients were diagnosed as vasculitic neuropathy in six patients, perineuritis in two patients, CIDP in two patients, and Lewis-Sumner syndrome in one patient, based on clinical features, laboratory data, electrophysiological investigations and nerve biopsies.
Two patients were diagnosed with vasculitic neuropathy, and one patient was diagnosed with CIDP, based on clinical findings, but were not confirmed by nerve biopsy. Nerve biopsies confirmed or supported clinical diagnosis in There are five clinical patterns of nerve injury in vasculitic neuropathy—mononeuropathy, MM, polyradiculoneuropathy, asymmetrical polyneuropathy and symmetrical polyneuropathy.
A definite diagnosis of vasculitic neuropathy is dependent on nerve biopsy Vital et al. MM is not the most common pattern in vasculitic neuropathy, being found in only about one-third of vasculitic neuropathy cases. Asymmetrical polyneuropathy or symmetrical polyneuropathy, especially axonal sensory-motor polyneuropathy, is the most common clinical pattern, being found in about half of cases Oh, ; Vital et al. G Proteins: Techniques of Analysis.
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