Neuroscience and headaches

  1. Glut-1 Deficiency
    Symptoms, age of onset, CSF findings, treatment, underlying mutation
    • Microcephaly, ataxaia, seizures, spasticity.
    • Seizures by 4 months
    • Low glucose which is why you do a ketogenic diet so the brain uses ketones for energy rather than glucose.
    • SLC2A1 mutation
  2. Kearns-Sayre
    Symptoms, inheritance, which of the mitochondrial electron transport chain are most often affected?
    • Progressive external ophthalmoplegia, generalised weakness, cardiac conduction abnormalities, retinitis pigmentosa, elevated csf glucose, endocrine disorders.
    • COMPLEX 1
  3. Which organs mediate vibration sense?
    Pacinian Corpuscles
  4. Which organs mediate position and dynamic touch?
    Meissners corpuscles.
  5. Which cells derive from the neural crest and where does the neural crest arise from.
    • Neural crest arises from the ectoderm
    • Neural crest derivatives are:
    • Schwann cells
    • Dorsal root ganglion
    • Melanocytes
    • Adrenal glands
    • Enteric nervous system
  6. Headaches, abdominal pain, basophilic stippling and wrist drop?
    What does this toxin do to you?
    • Lead poisoning
    • Affects porphyrin metabolism by inhibiting gamma-aminolevulinic acid leading to a microcytic anaemia.
  7. Painful paraesthesias, garlicky breath and thick deposits in his nails?
    What does this toxin do to you?
    • Arsenic 
    • Interferes with oxidative metabolism causing dying back of myelinated fibres i.e. painful paraesthesia
  8. Allopecia, autonomic neuropathy and cranial neuropathies?
    What does this toxin do to you?
    • Thallium
    • Interacts with the Na/K ATPase
  9. Muscle spasms, opisthotonus and seizures?
    • Strychnine - antagonist of glycine and Acetylcholine.
    • Found in pesticides, rodenticides and herbal remedies.
  10. How do benzodiazepines work?
    How do barbiturates work
    • Benzos - Increased frequency of GABA channel opening. 
    • Barbiturates - Increased duration of GABA channel opening
  11. What makes up the basis of the blood brain barrier?
    • Tight junctions between cells - The Zona Occludens
    • Astrocytic Podocytes also contribute.
  12. Which nominal 'brain structures' lack a BBB?
    • Posterior part of the pituitary
    • Pineal gland
    • Area postrema (where the CTZ is)
    • Vascular organ of lamina terminals (VOLT)
    • Subfornical organ
    • Median eminence
  13. If you see Fahrs on a CT what do you need to rule out?
    • Hypoparathyroidism
    • Pseudohypoparathyroidism
    • Hyperparathyroidism
  14. Cobblestone lissencephaly?
    • Neurons found in the meninges - essentially theyve traveled too far during migration.
    • Associated with several neuromuscular conditions.
  15. What are the neuronal migration problems?
    • Heterotopia - can be periventricular or band like and cause seizures.
    • Schizencephaly - Clefts between ventricles and the subarachnoid space without gliosis.
    • Lissencephaly - Few or no gyri and low number of cortical layers.
    • Pachygyria - Few, broad and thickened gyri
    • Polymicrogyria - Lots of small gyri
  16. How many layers are there in the cortex?
    Which layer are the pyramidal cells in?
    • 6
    • Pyramidal motor cells in layer 5
  17. How does gabapentin modulate pain?
    Modulates presynaptic alpha-4-delta calcium channels
  18. Where is the auditory cortex?
    Inferior temporal gyrus
  19. Unilateral autonomic signs in Trigeminal autonomic cephalgias are caused by activation of?
    Superior salivatory nucleus
  20. What is the typical duration of the following trigeminal autonomic cephalgias:
    1. Cluster
    2. Paroxysmal hemicrania
    3. SUNCT
    • 1. 15-180mins
    • 2. 2-30mins
    • 3. 1-600seconds
  21. Is there a gender dominance of the trigeminal autonomic cephalgias?
    • Cluster male preponderance
    • Paroxysmal hemicrania female
  22. Which medications are associated with PRES?
    • Tacrolimus
    • Cyclosporin
    • Avastin and any anti VEGF agent
  23. Which conditions are associate with PRES
    • Hypertension
    • Autoimmune conditions
    • Pregnancy
    • Eclampsia
  24. Which triptan has the longest half life?
    Frovitriptan
  25. What is the most common site for a CSF leak?
    Thoracic cord
  26. What is Kluver-Bucy syndrome
    Hyperorality, Hyperphagia and Hypersexuality

    Lesion of the amygdala bilat (or more commonly bilateral medial temporal lobes in HSV enceph)
  27. What is Mollaret meningitis?
    • Recurrent meningitis with HSV-2
    • May need oral valcyclovir
  28. Whats the problem with cycad nuts?
    • They come from plant that have cyanobacterium which produce BMAA (beta methylamino L alanine).
    • People in many parts of the world either turn these nuts into flour or eat animals which eat these nuts and then get Parkinsonism/ALS complex
  29. Which genes are associated with familial hemiplegic migraine?
    How does the presentation of familial hemiplegic migraine differ from sporadic hemiplegic migraine?
    • CACNA1A - Type 1 - assoc with cerebellar atrophy
    • ATP1A2 - Type 2
    • SCN1A - Type 3
    • All autosomal dominant

    • Familial presents earlier (age 11-13).
    • Sporadic will be in the latter teenage years.
  30. Where should white matter lesions be to make you consider CADASIL?
    What chromosome is cadasil on?
    Which gene is affected?
    • Anterior temporal poles (90%)
    • Corpus callosum
    • Extreme capsule

    • Chr 19
    • Notch-3
  31. After the cerebral hemispheres, which region is most often affected in PML?
    What does pathology show in PML?
    • Caudate head
    • Balloned oligodendrocytes with nuclear inclusion and
    • Bizzare nuclei
  32. Which vein is most commonly affect in CVST?
    Superior sagital sinus
  33. Whats the problem with topiramate?
    • Weight loss
    • Cant mix it with valproate because youll get hepatic encephalopathy
    • It could give you calcium phosphate kidney stones
    • It could give you angle closure glaucoma!
  34. Right upper limb weakness, agraphia, acalculia, finger agnosia, right left disorientation...whats the syndrome called and where is the lesion?
    • Gerstmann's syndrome 
    • Dominant inferior parietal lobule - encompassing the angular and supramarginal gyri
  35. Where does the lesion need to be to cause prosopagnosia?
    Non-dominant fusiform gyrus lesion
  36. Astereognosis?
    • Tactile agnosia
    • Lesion of the superior parietal lobe
  37. Exclusion criteria for thrombolysis?
    • Systolic>185
    • Diastolic>110
    • Bleed
    • Platelets<100,000
    • INR>1.7 or on a DOAC
    • hypoglycaemia
    • Intracranial aneurysm >10mm
    • Brain tumor
    • Infective endocarditis
    • GI bled within 21 days
    • Major surgery within 14 days
  38. Relative risk reduction of Warfarin in AF?
    Relative risk reduction of Aspirin alone in AF?
    • Warfarin 68%
    • Aspirin 21%
  39. Other name for sturge-weber?
    Encephalotrigeminal angiomatosis

    • Port wine stain is your trigeminal angioma
    • Ipsilateral leptomeningeal angioma which looks like a paucity of blood vessels with associated brain atrophy. 
    • Buphthalmos (eye enlargement and protrusion)
    • They can get intractable seizures and need hemispherectomy
    • Inheritance is sporadic
  40. Fabry's disease?
    • Acroparaesthesia (lancinating pains in fingers and toes)
    • Angiokeratomas (dark red or purple papules found around the groin or umbilicus)
    • Cardiac arrythmias and CCF
    • Autonmic dysfunction (anhidrosis, impotence, gutdysmotility)
    • Accumulation of sphingolipids
    • Deficiency of Alpha-galactosidase A
    • X-linked recessive
  41. Mortality in GBS is mainly due to?
    • Autonomic dysregulation!
    • Its the cardiac arrythmias and cardiac arrest that gets them.
    • People generally know to look out for resp dysfunction
  42. What ind of weakness is classic of border zone infarcts?
    Proximal limb weakness - man in a barrel
  43. Whats the best treatment for symptomatic, large, intracranial artery atherosclerosis?
    • Aspirin + Clopi + Statin
    • SAMPRIS protocol
  44. Borderzone infarct of the dominant lobe leads to?
    Transcortical aphasia with intact repetition
  45. When does peak vasospasm occur in Aneursymal SAH?
    4-14 days
  46. How many first degree relatives need to have had an SAH or Aneurysm in order to screen asymptomatics?
    2
  47. Complications of SAH?
    • Vasospasm
    • Re-bleed
    • Seizures
    • Hydrocephalus
    • Hyponatraemia
  48. Which conditions are associated with SAH?
    • ADPKD
    • Moya Moya
    • Co-arctation of the aorta
    • NF1
    • Pompe's
    • Fibromuscular dysplasia
  49. Features of Expressive dysphasia?
    (Broca's)
    • Non-fluent Staccato speech
    • Cannot name or repeat
    • Comprehension preserved
  50. Features of Receptive aphasia?
    (Wernicke's)
    • Fluent but nonsensical speech
    • Cannot name or repeat
    • Comprehension badly impaired
  51. Conduction aphasia?
    (Arcuate fasiculus)
    • Impaired repetition
    • Comprehension intact
    • Mild expressive difficulty
  52. Transcortical aphasia?
    • The only one where repetition is preserved.
    • Caused by watershed infarcts affecting the TPO junction.
  53. Where is Broca's and where is Wernicke's?
    • Broca's: posterior part of inferior frontal gyrus
    • Wernicke's: Posterior part of the superior temporal gyrus.
  54. Facts about fibromuscular dysplasia?
    • It only effects the extracranial vessels
    • Predisposes to Carotid artery dissection.
    • Looks like a string of beads on angio.
    • 65% are bilateral. 
    • Most common presenting feature is Hypertension because the renal artery is the most commonly involved.
  55. Most common location ofr hypertensive bleed?
    • Putamen
    • Thalamus
    • Cerebellum
    • Ventral part of the pons
  56. What is a highly sensitive marker for Diffuse axonal injury and which imaging modalities show DAI best?
    • CSF B Amyloid 
    • SWI/GRE sequences show micro-haemorrhages at GWMJ, Corpus callosum and brainstem
  57. How many half lives of sedative medication need to be allowed before confirmation of brain death?
    5 half lives
  58. What are the differences between critical illness myopathy and neuropathy?
    • Reflexes and sensation are preserved in myopathy. Absent in neuropathy.
    • NCS shows prolonged CMAP in myopathy. Normal in neuropathy.
    • Loss of type 2 myofibres in myopathy.
    • Axonal loss in neuropathy.
  59. Everyone knows methanol makes you go blind....what else does sit do?
    • Haemorrhagic necrosis of putamen 
    • The blindness is optic atrophy.

    Methanol is converted to formaldehyde and then formic acid...thats right, the stuff ants use to burn you.
Author
vb406
ID
349732
Card Set
Neuroscience and headaches
Description
Neurology revision cards
Updated