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Neuroimmunology
| @NeuroFOD | @NeuroFOD |
|---|---|
| Neuroimmunology | Neuroimmunology |
| Optic neuritis associations | uL = MS. bL = NMO, MOG, Sarcoid, Lupus |
| Young female with red desaturation, +APD, +pain | Optic neuritis |
| Do you need MRI for optic neuritis? | Not for diagnosis. But must get MRI brain to assess for other lesions |
| Optic neuritis treatment | IV steroids (ONTT trial showed oral steroids are inferior). Can also do ACTH gel (corticotropin) |
| Post-infection ascending neuropathy, +hyperreflexia | Transverse myelitis. Will have AIDP-like neuropathy but +hyperreflexia and +sensory level |
| Transverse myelitis treatment | Steroids. Some trials show they work better than PLEX and IVIG |
| Multiple Sclerosis pathophysiology | Myelin antigen incorrectly tagged by CD8 T-cells -> B-cells/mpgs -> reactive astrocytic inflam |
| White woman with MS vs black woman with MS | Black women have worse radiological progression AND worse clinical progression |
| Multiple Sclerosis characteristic symptoms | Focal numb & upper motor weak. Also optic neuritis, INO, trigeminal neuralgia, Lhermite's sign |
| Multiple Sclerosis hug | Chest tightness in MS. Not related to MS flare |
| McDonald's Criteria | This is very high yield. Refer to Neuroimmunology Review |
| MS Radiologically Isolated Syndrome criteria | No clinical attacks. Only evidence of typical hyperintense lesions on MRI FLAIR |
| Typical lesion areas for MS (5) | Juxtacortical, periventricular, pontine, cerebellar, spinal cord (<3 spinal segments) |
| Typical lesion areas for NMO | Brainstem (peri- 3rd/4th ventricles), spinal cord (>3 spinal segments "longitudinally extensive") |
| Multiple Sclerosis histopathology | CD8 T-cells, macrophages, antibodies from B-cells (to myelin), and complement |
| Multiple Sclerosis enhancement vs abscess/tumor | MS & other demyelinating disorders = open-ring. Abscess and tumor = closed ring |
| MR Spect findings in Multiple Sclerosis | Decreased NAA / Cr ratio |
| Uthoff phenomenon | Worsening MS symptoms with heat/stress/triggers. Not a true flare |
| MS Clinically Isolated Syndrome criteria | 1 clinical attack + 1 enhancing lesion only. No attack hx, no old lesions, no OCBands |
| Most commonly affected executive function in MS | Attention. More affected than memory or decision making etc. |
| What happens to MS in pregnancy? | Decreased attacks while pregnant, but increased attacks after delivery |
| Which meds to use for MS flare in pregnancy? | Steroids only. No IVIG (d/t hypercoagulability) and no PLEX |
| Which meds to use for MS maintanence in pregnancy? | Glatimir acetate is safe. Some research says interferon, DMF, and Natalizumab may be safe too |
| MS RIS treatment | None until MS identified. Note: must get MR C-spine (if lesions = worse prognosis) |
| MS CIS treatment | Treat as if it's MS. Early treatment reduces progression and disability |
| MS spasticity treatment | Tizanidine, dantrolene, baclofen |
| MS urinary retention treatment | Tolterodine, oxybutynin |
| MS gait instability treatment | Dalfampiridine (K channel blocker = keep neuron depolarized for longer) |
| MS pseudobulbar affect treatment | Dextromethorphan + quinidine (NMDA Antag). Combination pill commonly known as Nudexta |
| How much Vitamin D should MS women take? | 2000 international units daily. More if they are deficient |
| Crutz-Peters cells | Tumefactive MS |
| Marburg MS | Marburg MS = Tumefactive MS = single tumor-like demyelinating lesion |
| Tumefactive MS MRI | Single tumor-like demyelinating lesion with incomplete (open-ring) enhancement |
| MS + seizures, loss of conciousness | Balo Concentric MS = MS + fulminant meningitis. MRI shows edema + necrosis |
| Child, post-viral widespread demyelination | ADEM |
| MS lesions different MRI sequestions | T1=hypointense "black holes", T2=hyperintense, DWI/ADC=+restriction, Contrast=open-ring |
| Typical lesion areas for ADEM | Asymmetric large juxtacortical/periventricular lesions. Involve thalamus (unlike MS/others) |
| ADEM treatment | Steroids, IVIG/PLEX. No abx necessary as it is post-infectious autoimmune |
| NMO typical patient demographics | 40s, Asian/Black women (unlike MS = white women), especially if other autoimmune disorders |
| Area postrema syndrome | Incontrollable nausea/vomiting due to midbrain lesion. A/w NMO |
| MS vs NMO on biopsy | MS = primarily CD8 T-cells. NMO = primarily Aqp4 antibody B cells. But there's lots of overlap |
| NMO treatment | 1st line is azathioprine, mycophenolate, rituximab. Can also repeat IVIGs. New = Eculizumab |
| Eculizumab | Complement inhibitor (inhibits C5 cleavage). Treatment for NMO |
| Where Aqp4 located? | On astrocyte foot processes that make up the BBB |
| Aqp4 sensitivity and specificity | Actually has better sensitivity and specificity for NMO if measure in serum, more than CSF |
| Nausea/vomit/dizzy, altered consciousness, CN palsies | Consider Bickerstaff brainstem encephalitis. Anti-GQ1 |
| Oral ulcer, genital ulcer, uveitis, brainstem/CN/cerebellum | Behcets Syndrome (unexplained multisystem vasculitis). Seen in child, male, mediterranean |
| Behcets syndrome association | Multisystem vasculitis, including pulmonary artery aneurysms and brain CSVT |
| Behcets syndrome treatment | Typically very responsive to steroids |
| CLIPPERS | Chronic Lymphocytic Inflammation w/ Pontine Perivascular Enhancement Responsive to Steroids |
| MRI peppering of the pons | CLIPPERS |
| Episodic diplopia, ataxia, dysarthria | CLIPPERS (pontine perivascular inflammation) |
Created by:
amitchaudharimd
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