Zhang, Tony

ABSTRACT Background and Aims Nonsystemic vasculitic neuropathy classically presents as a painful asymmetric axonal neuropathy, multiple mononeuropathies or radiculoplexus neuropathy. Demyelinating electrophysiologic features are rare and may lead to misdiagnosis. We describe a patient with biopsy‐proven vasculitic neuropathy presenting as a severe symmetric demyelinating polyradiculoneuropathy. Methods Clinical, electrophysiologic, imaging, laboratory, and histopathologic findings are presented. Results A 57‐year‐old man developed acute ascending weakness, sensory loss, facial weakness, and areflexia following a febrile illness, with initial improvement before developing recurrent neurological decline 6 weeks after initial symptom onset despite treatment with intravenous immunoglobulin and plasma exchange. Cerebrospinal fluid protein was elevated. Nerve conduction studies demonstrated prolonged distal motor latencies, slowed conduction velocities, conduction block, and prolonged blink reflex latencies, fulfilling 2021 European Academy of Neurology/Peripheral Nerve Society electrodiagnostic criteria for chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). MRI demonstrated mild but diffuse lumbosacral plexus enlargement and T2 hyperintensity. Sural nerve biopsy ultimately demonstrated evidence of epineurial inflammation and microvasculitis with ischemic nerve injury, accompanied by both increased rates of axonal degeneration (12%) and segmental demyelination (9%) on teased fiber analysis. Treatment with corticosteroids and rituximab resulted in complete neurological recovery. Interpretation Vasculitic neuropathy may closely mimic CIDP clinically, radiologically, and electrophysiologically. Clues to the vasculitis diagnosis were prominent neuropathic pain, dense denervation on electrophysiology, and poor response to typical CIDP treatment. Peripheral nerve biopsy remains a critical tool in the evaluation of atypical or treatment‐refractory inflammatory neuropathies.

This case report describes a 65-year-old man who experienced complete remission of cavin-4 immunoglobulin G (IgG) rippling muscle disease after receiving rituximab therapy.

Background Spontaneous intracranial hypotension (SIH) results from cerebrospinal fluid (CSF) leakage due to spinal dural tears or CSF–venous fistulas. Orthostatic headache is the hallmark presentation, though severe downward displacement of the brainstem may lead to altered consciousness or coma. Definitive treatments include targeted epidural blood patches, venous embolization, or surgical repair. Methods This article reviews the role of the Trendelenburg position as a temporizing measure in the acute management of SIH. We describe the correct technique, physiologic rationale, and practical considerations for its application, with attention to both therapeutic and diagnostic utility. Discussion Positioning the patient with the feet elevated above the head can reduce brain sag and provide short-term symptomatic relief while awaiting definitive treatment. Although the Trendelenburg position is widely used in practice, supporting evidence remains limited, and clinicians must be aware of its benefits, indications, and inherent limitations. Its appropriate application may assist in stabilizing patients with acute or severe SIH, particularly those with impaired consciousness, until more definitive interventions are pursued.