Case Presentation: A 57-year-old male came to the hospital after he noticed dysarthria and progressive bilateral arm and leg weakness, with sensory changes that were progressive over 2 months. At the time of his presentation, his functional status had diminished- he had to use a cane to ambulate. His medical history was pertinent for HIV, with undetectable viral load. Patient received his Covid-19 vaccine 2 weeks before symptom onset. His physical exam was notable for distal more than proximal multimodal sensory loss and diffuse hyporeflexia, decreased bulk of his quadriceps and his toes had a hammertoe appearance. Multiple tests for motor sensory neuropathy came out to be negative. Lab workup was unremarkable for nutritional deficiencies, heavy metals or, thyroid abnormalities. Paraneoplastic autoantibody and MRI lumbar spine were unrevealing. Patient underwent fluoroscopic lumbar puncture which revealed albumino-cytologic dissociation. The CSF breakdown was as follows: elevated protein to 88.7, Glucose 61 mg/dl, WBC count 1 /uL, neutrophil count 8%, lymphocyte 60%, monocyte 32%. Fluid analysis revealed presence of COVID antibody with no neoplastic cell found. Electromyography and nerve conduction studies revealed a severe demyelinating length-dependent sensorimotor polyneuropathy with only mild evidence of active denervation on the needle exam. Patient was diagnosed with Chronic Inflammatory Demyelinating Polyneuropathy (CIDP). Patient was treated with IVIG for 5 days and noticed a remarkable improvement in his dysarthria and also improvement in his functional status.
Discussion: Chronic inflammatory demyelinating polyneuropathy (CIDP) is an acquired, immune-mediated neuropathy affecting peripheral nerves and nerve roots. CIDP has variable manifestations. Pathophysiology is inflammatory demyelination. Diagnosis should be considered in patients presenting with polyneuropathy with areflexia, particularly when weakness predominates and affects proximal and distal muscles simultaneously and symmetrically. Cerebrospinal fluid analysis is recommended and albumino-cytologic dissociation is a hallmark of CIDP. Nerve conduction studies can reveal demyelinating neuropathy. Immune-modulatory treatment using either intravenous immune globulin (IVIG), plasma exchange, or glucocorticoids are effective [1-6]. Our case depicts a patient with symmetrical polyneuropathy with sensory abnormalities. Lumbar puncture revealed albumino-cytologic dissociation and nerve conduction studies revealed severe demyelinating length-dependent sensorimotor polyneuropathy. While the etiology of our patient’s CIPD remains unknown, the leading differential causes were secondary to the Covid-19 vaccine or HIV. The prognosis of CIDP is generally favorable, but data is limited [7-8].
Conclusions: CIDP diagnosis should be considered in patients who present with symmetric, motor-predominant peripheral neuropathy that causes both proximal and distal weakness, sensory impairment that is usually greater for vibration and position sense than for pain and temperature sense, and areflexia. The course can be progressive or relapsing-remitting. There is no gold standard test for diagnosis, rather a combination of features can be used to diagnose CIDP. Treatment with IVIG should be commenced if diagnosis is suspected to get a rapid response and slow disease progression.