Many of my neurology colleagues feel uneasy when admitting a patient with severe, chronic (> 2 months) rapidly progressive peripheral neuropathy of uncertain etiology. While there are more than 100 causes of neuropathy, the most likely causes in this clinical setting can be narrowed down to the six below:

🔺 Chronic Inflammatory Demyelinating Polyradiculoneuropathy (CIDP), including autoimmune nodopathies

🔺 Amyloidosis

🔺 Paraneoplastic syndrome, including POEMS syndrome

🔺 Vasculitis, including radiculoplexus neuropathies

🔺 Lymphoma or carcinomatous meningitis

🔺 Nutritional deficiencies

#NeuropathyBites
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1/x It’s important to note that this post refers to patients with moderate to severe disability caused by neuropathy, often dependent on wheelchairs and doesn't include patients with multifactorial gait disorder. In addition, some electromyographers report “severe neuropathy” based solely on lower extremities conduction studies, so caution is advised when using nerve conductions to define the severity of a neuropathy.

Another critical point is that patients are not good at differentiating progression versus no improvement of subacute/chronic weakness, so use landmarks like starting gait aids, the ability to stand up from the toilet without using the hands or help of someone, and falls, foot drop, wrist drop, abnormal gait, or inability to do something in their daily routine when they started. Be mindful that GBS, by definition, does not progress beyond 4 weeks.

Amyotrophic Lateral Sclerosis (ALS) is a more common cause of hospital admissions than all the conditions listed above, so a thorough history and detailed examination of the patient are essential. Bulbar symptoms/signs and upper motor neuron signs are highly suggestive of ALS. Moreover, up to 20% of ALS patients may also exhibit concomitant peripheral neuropathy; therefore, be careful about “motor-predominant polyradiculoneuropathies” that present with only mild sensory involvement.

2/x

In celebration of the legendary career of Professor Peter J. Dyck, who officially retired last month, I kick off today this series with a hidden gem: The 10 P's in the characterization and differential diagnosis of peripheral neuropathy.

#NeuropathyClassics

#DyckPapers

1/
Modern medical educators may not agree with a 10 point mnemonic but this was the 80s/90s and Dr. Dyck is a very thoughtful and comprehensive neurologist.

neurology.org/doi/10.1212/WN…

The first “P” (P1) is for Pattern:

- Anatomical and temporal localization of the disease.

- Anatomical pattern includes mononeuropathy, monoradiculopathy, multiple mononeuropathies, plexopathy, polyneuropathy or polyradiculoneuropathy.

- Temporal pattern considers onset (acute, subacute, chronic) and course (monophasic, recurrent,
progressive).

2/

Acute nutritional axonal neuropathy (dry beri-beri) is more common than many believe.

In patients with malnutrition, intractable vomiting, heavy alcohol use, or a poorly balanced diet, this condition is more likely than Guillain-Barré Syndrome (GBS). #NeuropathyBites

1/ These patients need IVT(thiamine) and not IVIg. I treat them with 500 mg IV q8h for 3 days, then 100 mg daily orally, and supplement other vitamins as needed.

The neuropathy is usually more distal and sensory predominant compared to GBS, though it can mimic GBS exactly.

2/

🚨Check out our latest work on vasculitic myopathy @GreenJournal! A fantastic collaboration between @MayoClinicNeuro and #MayoRheum. Thank you, @ElieNaddaf3, for the incredible mentorship, and @MdWarrington and #MattKoster for the help. Breakdown ⬇️ 1/7
neurology.org/doi/pdf/10.121… • We report 25 patients vasculitic myopathy

• Primary systemic Vasculitis: 40% (ANCA vasculitides most common)

• Secondary systemic vasculitis: 48% (RA most common)

• Nonsystemic vasculitic myopathy: 12%

2/7

Feels so good to be back to #Neurology. Today I had the pleasure to give #Neurologymorningreport on Necrotizing Autoimmune Myopathy #NAM. #MedTwitter follow below a few pearls I shared with the team @ErsidaBuraniqi @nzalewski2. THREAD. #NAM is an autoimmune myopathy characterized by severe proximal weakness, myofiber necrosis with minimal or no inflammatory infiltrates on muscle biopsy, and infrequent extra-muscular involvement.