📚 Chemo: platins, taxanes, bortezomib, ICIs, ART: didanosine, stavudine, zalcitabine, Abx: metronidazole, linezolid, quinolones, nitrofurantoin, TB: isoniazid, dapsone, Amiodarone

⚪ Just like we give high-dose IV thiamine for Wernicke-Korsakoff, empiric IV thiamine should also be given for acute polyneuropathy if any signal at all for malabsorption/malnourishment (”IVT > IVIg”)

🚰 Lumbar Puncture (@MarcusVPinto)? The utility of the LP for acute polyneuropathy is not to confirm AIDP (i.e. Guillain-Barre), but to rule out other potential diagnoses, such as W. nile virus, other polio-like infections, sarcoidosis, & leptomeningeal malignant spread. Albuminocytologic dissociation is non-specific & only occurs in 50% of AIDP patients within the 1st week, & ~80% of patients after the 1st week. The sensitivity increases to about ~90% after several weeks. The lack of specificity derives from numerous reasons for ↑ CSF protein > 45 mg/dL, including diabetes, spondylosis, & various inflammatory neuropathies. More importantly, if CSF protein is high but CSF cell count is > 50 cells/mm^3, this is a signal not for AIDP, but for infectious polyradiculitis or infiltrative process (e.g. leptomeningeal malignant spread)

⚡ EMG/NCS? UpToDate authors recommend this for: 1) High suspicion polyneuropathy w/o a clear etiology 2) Severe vs. rapidly-progressive 3) Atypical features (i.e. asymmetry, non-length dependent, motor predominance, acute onset, dysautonomia). Overall, this is helpful to determine myopathy vs. neuropathy, axonal vs. demyelinating, polyneuropathy vs. other neuropathy (e.g. lumbar stenosis mediated radiculopathy, myelopathy)

• Autoimmune screen: ANA, CCP/RF, SSA/SSB, Cryoglobulins/HCV/HBV, TTG/Gliadin

• Nodo-paranodopathy antibodies: ganglioside panel, Demyelinating neuropathy panel, Motor neuropathy panel

• Paraprotein screen (VEGF, IL-6, Gammopathy panel) & Paraneoplastic antibody panel (anti-Hu, numerous others)

• Heavy metal screen: Pb, Hg, As, Cd, Th

• Nerve biopsy (AFB stain & culture for leprosy, Congo stain for amyloidosis, H&E for vasculitis & sarcoidosis) & Fat pad aspirate

• Porphyria screen: urine porphobilinogen/porphyrin

• Genetic sequencing: inherited TTR amyloidosis, other hereditary

• Cervical myelopathy: consider if weakness of all 4 limbs ⊕ mixed UMN/LMN signs (as in ALS)

Motor Neurons 🎭

• ALS: a more common cause of hospital admission than all of the 3rd-pass causes. Requires thorough examination for bulbar & UMN signs. Of note, up to ~20% of ALS patients may also exhibit peripheral neuropathy (i.e. patient may be labeled as having “motor-predominant polyradiculopathy”)

• Ganglionopathy (Sensory Neuronopathy) 2/2 ___
• Sjogren's & SLE (ANA, SSA/SSB), Celiac (TTG, Gliadin)
• Malignancy (Pan scan → PET/CT)
• Antibody-mediated (Hu, CV2/CRMP-5)
• B6 & Platinum-chemotherapy toxicity
• HIV, EBV, VZV

⚪ Classically, patient has "patchy" sensory loss, but any pattern of sensory loss possible since dorsal root ganglia contain input from multiple roots. Supportive findings include gait ataxia without cerebellar signs (exception = autoimmune nodopathies affecting cerebellum), & "give way" weakness that ↑ on eye closure & ↓ on visual coaching

🚨 Ganglionopathy is often misdiagnosed as functional neurologic disorder due to patients reporting being too weak to function & having "give way" weakness (because if they look at their limbs, they will be able to overcome the poor coordination with visual supplementation)