Tag Archives: neuroimaging

MRI evolution of Cerebral Abscess




Criner, G., Barnette, R. and D’Alonzo, G. (2010). Critical Care Study Guide. Dordrecht: Springer.



Encephalopathy Work-up

Screening tests

  • Serum glucose, electrolytes, calcium/phosphorus, uric acid, lactate and pyruvate, liver, renal and thyroid function tests, blood gasses
  • Prolactin levels (10 to 20 min after suspected seizure, diagnosis seizure vs. psychogenic nonepileptic seizure)
  • Serum CK
  • ANA, ENA, ANCA, RF, complement, ACE, anti-thyroglobulin and anti-thyroperoxidase antibodies (Hashimoto disease), autoantibody panel (thyroid antimicrosomal, antiparietal),  immunoglobulins
  • Serum ceruloplasmin and copper, 24h urinary copper, slit lamp, liver biopsy (WD)
  • CBC, ESR, CRP, plasma fibrinogen
  • Coagulation profile (protein C and S, ATIII, Factor Leiden V, APLS, anticardiolipin)
  • Serum vitamin B12 and folic acid
  • Serum cortisol, PTH and osmolality.
  • Serology: HIV, HSV, adenovirus, CMV, Coxsackie, polio, echovirus, hepatitis (A,B,C), parvovirus B19, mycoplasma, toxoplasma, VDRL, cysticercosis
  • Blood and urine organic acids and carnitine
  • Chest X-ray
  • PPD
  • Echocardiogram
  • EEG (non-convulsive status epilepticus), VEP, EMG/NCVs
  • Brain MRI, MRA
  • Conventional angiogram (CNS vasculitis)
  • serum ammonium


  • Besides routine analysis (chemistry, cell count, smear and stainings): lactate and pyruvate (mitochondrial disease), oligoclonal bands, IgG index, VDRL, viral (measles titer), fungal, PCR (T. Whippleii, JC virus, HSV, CMV, VZV), Ziehl staining, repeated cytology,
  • anti-thyroglobulin and anti-thyroperoxidase antibodies (Hashimoto disease).

Specific investigations


  • 14-3-3 protein (CJD) (stable at room temperature and can be sent by regular mail)
  • Aminolevulinic acid, porphobilinogen, uroporphyrins, coproporphyrin
  • Antineural nuclear antibodies (ANNA-1(=Anti-Hu), ANNA-2 (=anti-Ri), ANNA-3, Purkinje cell cytoplasmic antibodies (PCCA-1 (=anti-Yo), PCCA-2, PCCA-Tr and mGluR1), plasma membrane cation channel antibodies (CV2/CRMP-5, Ma1, Ma2/Ta, amphiphysin, striational, voltage gated calcium channels (VGCC) and voltage gated potassium channels (VGKC), anti-NMDA-R (NR1 and NR2) antibodies.
  • Methylmalonic acid, VLCFA, arylsulphatase, homocysteine


  • Conjunctiva (sarcoidosis),
  • Small bowel (Whipple disease)
  • Skin (SLE, vasculitis, CADASIL)
  • Brain biopsy

COMA Algorithm (ENLS 2017)

Neurologic Etiologies of Coma

Toxic-Metabolic Etiologies of Coma


“Acute Encephalopathy Work-Up.” Neuroweb.us. http://www.neuroweb.us/Chapters/acute%20encephalopathy/work_up.htm, 2017. Web. 18 Aug. 2017.

Posterior Cerebral Artery Branches



4 anatomic segments of the PCA:

  1. P1 segment: from tip of basilar to origin of PComm
  2. P2 segment: from Pcomm to dorsal midbrain
    1. P2A – anterior segment
    2. P2P – posterior segment
  3. P3 segment: from lateral quad cistern at origin of post temporal artery to ant limit of calcarine fissure
  4. P4 segment:  terminal cortical branches of PCA after takeoff of parieto-occipital and calcarine arteries



AJNR Am J Neuroradiol. 2001 Jan;22(1):27-34. “Aneurysms of the posterior cerebral artery: classification and endovascular treatment.”   Ciceri EF1, Klucznik RP, Grossman RG, Rose JE, Mawad ME.

Choroid Plexus Blood Supply





Haines, Duane E. Neuroanatomy : An Atlas Of Structures, Sections, And Systems. 8e, 2012.

Digital Map of PCA Infarcts

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Phan, MBBS, FRACP, T. G. et al. “Digital Map Of Posterior Cerebral Artery Infarcts Associated With Posterior Cerebral Artery Trunk And Branch Occlusion”. Stroke 38.6 (2007): 1805-1811.

Digital atlas of MCA territory infarction

The color refers to the frequency of infarction at each voxel. The highest frequency of infarct occurrence is in the centrum semiovale and striatocapsular and insular regions.


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Phan, T. G. et al. “A Digital Map Of Middle Cerebral Artery Infarcts Associated With Middle Cerebral Artery Trunk And Branch Occlusion”. Stroke 36.5 (2005): 986-991.

Delayed Cerebral Ischemia (Definition)



Delayed Cerebral Ischemia:

Focal (hemiparesis, aphasia, hemianopia, or neglect) or global (2 points decrease on GCS) neurological impairment lasting for at least 1 hour and/or cerebral infarction, which:
▪ Is not apparent immediately after aneurysm occlusion
▪ Is attributable to ischemia
▪ Is not attributed to other causes (i.e. surgical complication, metabolic derangements) after appropriate clinical, imaging, and laboratory evaluation


Cerebral infarction:

Presence of cerebral infarction on CT or MR scan of the brain within 6 weeks after SAH, or on the latest CT or MR scan made before death within 6 weeks, or proven at autopsy; that is:
▪ Not present on the CT or MR scan between 24 and 48 hours after early aneurysm occlusion
▪ Not attributable to other causes such as surgical clipping or endovascular treatment
▪ Not due to a nonischemic lucency related to a ventricular catheter, intraparenchymal hematoma, or brain retraction injury



Francoeur, Charles L. and Stephan A. Mayer. “Management Of Delayed Cerebral Ischemia After Subarachnoid Hemorrhage”. Critical Care 20.1 (2016): n. pag. Web.