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Cognitive Disorders
| @NeuroFOD | @NeuroFOD |
|---|---|
| Cognitive Disorders | Cognitive Disorders |
| Types of memory | Declarative = facts (episodic=events, semantic=language), procedural = motor, implicit = skills |
| Forgets meaning of a word. Type of memory? | Semantic |
| Forgets what happened yesterday. Type of memory? | Episodic |
| Implicit memory example | Forgetting a non-motor skill. Motor skills = procedural memory |
| Fluctuating attention and cognitive deficits | Delirium. Often reversible |
| Delirium treatment | Antipsychotics are temporizing, but do not decrease duration of delirium. Avoid anticholinergics |
| TGA patient demographics | 50-80yo, no sex preference, not necessary any comorbidities |
| TGA pathophysiology | Unclear. But thought to be due to hypoperfusion of hippocampi. 7T MRI will show +DWI signal |
| Sudden memory loss, back to normal in 24 hours | Transient Global Amnesia TGA |
| TGA vs Dissociative Fugue | TGA = neurological = preserved awarness of self. Fugue = psychiatric = cannot recognize self |
| MCI definition | Reduced memory (more than normal aging) but no deficits on ADLs and normal cognition |
| Risk factor for MCI progression to dementia | Family history. Others like age etc have less evidence |
| Alzheimers patient demographics | Black/hispanic more likely. Low education/socioeconomic status more likely |
| Alzheimers pathophysiology | Microangiopathy from DM/HTN/HLD/Smoking -> buildup of Tau |
| Alzheimers histopathology | Intracell Tau neurofibrillary tangles. Extracell APP beta-Amyloid senile plaques. Hirano bodies |
| Alzheimers CSF | Has high Tau but low beta-Amyloid (frequently tested) |
| What molecule is used in Alzheimers FDG-PET scans? | CompB |
| Alzheimers MRI | 1st = medial parietal, posterior cingulate. Then parietotemporal atropy |
| FDG-PET \/metabolism in parietotemporal | Alzheimers |
| FDG-PET \/metabolism in occipital | Lewy-Body Disease |
| FDG-PET \/metabolism in frontotemporal | Fronto-Temporal Dementia |
| What is the function of Tau? | Microtubule transport. Dysfunction = impaired intracellular transport of proteins/neurotransmitters |
| Alzheimers genes | Chrm 21 APP. Chrm 14 PSEN1. Chrm 1-PSEN2. Chrm 19 APOE epsilon 4 |
| 1st type of memory damaged in Alzheimers | Recent memory. Then episodic -> semantic -> language |
| Alzheimers treatment | ACEi (donepezil, galantamine, rivastigmine), NMDA-antag (memantine). New = Adacanumab |
| Adacanumab side-effect | Diffuse cerebral edema |
| Alzheimers associated conditions | Cerebral Amyloid Angiopathy CAA. Down syndrome |
| Best predictor of driving in Alzheimers dementia | Cognitive test. 2nd is caregiver perception. Least reliable is what patient self-assesses |
| Where is Tau located? Where is beta-amyloid? | Tau is intracellular. Beta-amyloid is extracellular |
| Hirano bodies | Actin filaments. A/w Alzheimers |
| Early Onset Alzheimers | Will affect multiple cognitive domains. Still non-hereditary is most common |
| Posterior Cortical Atrophy | Occipital hypometabolism and atrophy. Largely visual memory loss (faces, people, driving, etc) |
| FTD gene | C9orf72 and TDP42 if with ALS. Others include Chrm 17q21 MAPT, and PGRN |
| What chromosome is TDP43 located on? | ALS + FTD. Located on chromosome 9 |
| Personality changes, disinhibition, apathy, dementia | Fronto-Temporal Dementia |
| Hyperphosphorylated Tau | Fronto-Temporal Dementia |
| FTD histopathology | Spherical hyperphosphorylated Tau. Unlike Alzheimers, FTD is not tangles and has no amyloid |
| What is ubiquitin? | Protein tag. Tagged cells will undergo autophagocytosis |
| Picks dementia | Variant of Fronto-Temporal Dementia. More apathy/abulia. A/w Kluver-Bucy |
| Primary Progressive Aphasia | Variant of Fronto-Temporal Dementia. More temporal language deficits |
| MRI "knife-edge" sylvian fissure | Temporal atrophy. Consider Primary Progressive Aphasia variant of FTD |
| Word-finding difficulties, parkinsonism, temporal atrophy | Primary Progressive Aphasia -- Nonfluent = L anterior perisylvian fissue |
| Vocabulary/naming difficulties, temporal atrophy | Primary Progressive Aphasia -- Semantic = L>R anterior temporal lobe |
| Word-finding difficulties, dysphasia, Alzheimers | Primary Progressive Aphasia -- Logopenic = L posterior temporal and inferior parietal |
| Sneddon syndrome | Slowly progressive blockages of small/medium arteries -> vascular dementia |
| Binswanger disease | Traditional risk factors (DM/HTN/etc) -> white matter disease -> vascular dementia |
| Vascular dementia treatment | Start Donepezil, not just control risk factors. Donepezil is FDA approved for vascular dementia. |
| CJD protein | PrPsc prion protein from PRNP gene on Chromosome 20p |
| CJD inheritance | Overwhelmingly due to spontaneous mutations in protein misfolding. Rarely genetic |
| Does immunosuppression increase risk of CJD? | No. CJD is not autoimmune or infectious, it is spontaneous protein misfolding |
| Rapid dementia, hallucinations, myoclonus, ataxia | Creutzfeldt-Jacob disease CJD = Prion disease |
| EEG 1Hz repetitive sharp-wave | 1Hz is often seen in CJD |
| CJD CSF | Often normal, can sometimes mimic Alzheimers (increased Tau, Hirano bodies) |
| 14-3-3 | Marker for CJD |
| Most sensitive test for CJD | MRI showing cortical diffusion restriction ("cortical ribboning"), +basal ganglia and pulvinar |
| Most specific test for CJD | RT-Quic PCR. More specific that 14-3-3 or EEG 1Hz findings |
| CJD histopathology | Spongiform. Neuronal loss without any inflammation |
| Do you have to report CJD to public health authorities? | No. It is generally not contagious unless tissues/organs are consumed in cannabalism |
| Fatal Familial Insomnia FFI | Variant of CJD with intractable insomnia |
| CJD variants | Fatal Familial Insomnia. Kuru. Mad cow |
| Subacute fluctuating dementia, seizures | Check thyroid. Specifically TPO antibodies. Differential also autoimmune/paraneoplastic |
| Incontinence + gait difficulties + dementia | "Wet, wobbly, wachy" of normal pressure hydrocephalus |
| Magnetic gait | Normal pressure hydrocephalus |
| Normal pressure hydrocephalus test | LP for CSF drainage. Assess gait pre- and 1-hour post-LP |
| Normal pressure hydrocephalus treatment | Repeat LPs or shunt. Note: only helps gait/falls - no impact on cognition |
Created by:
amitchaudharimd
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