- Past history of TGA
- Advanced Age
- Migraneous Headaches
- full neuro exam (CN, sensory, motor, cerebellu, reflexes)
- memory exam (explicit memory loss, intact implicit memories)
- test immediate (intact) vs delayed recall (impaired)
- test attention span with serial 7’s WORLD backwards (intact)
- test procedural memory (intact)
TGA – all symptoms should resolve under 24 hours.
- if no resolution in 24 hours – requires broader investigation (MRI/CT, LP, EEG)
- imaging: MRI preferred over CT unless suspicion of acute ischemic stroke
- EEG to r/o seizures
- work-up patients with no witness at onset, <50 years old (rarer), high risk (immunocompromised, drug / ETOH use, abnormal VS)
- thiamine if h/o ETOH abuse
- hold meds that can cause amnesia (benzos)
- observe in ED OBS UNIT or inpatient x 1-2 days until resolution of symptoms
- serial neuro exams until patient returns to normal
- 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
- RPR, TPHA
- 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
- 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).
- 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
“Acute Encephalopathy Work-Up.” Neuroweb.us. http://www.neuroweb.us/Chapters/acute%20encephalopathy/work_up.htm, 2017. Web. 18 Aug. 2017.
Proposed Mechanism for HCP causing Takotsubo:
Sympathetic control of the heart is mediated by hypothalamic nuclei that abut the walls of the third ventricle. Specifically, dysfunction of PVN and DMN has been linked to catecholamine-induced myocardial necrosis. Hydrocephalus may disrupt these centers, although intracranial hypertension may not be necessary for this to occur.
*Paraventricular nucleus (PVN): TRH release, CRH relesase, oxytocin release, vasopressin release, somatostatin release
**Dorsomedial nucleus (DMN): BP, HR, GI stimulation
Gharaibeh, Kamel, Jackie Scott, and Nicholas A. Morris. “Neurogenic Stress Cardiomyopathy Precipitated By Acute Hydrocephalus After Aneurysmal Subarachnoid Hemorrhage.” Neurocritical Care (2017): n. pag. Web. 14 Aug. 2017.
“Hypothalamus.” En.wikipedia.org. N.p., 2017. Web. 14 Aug. 2017.