Category Archives: Uncategorized

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
  • 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
  • PPD
  • Echocardiogram
  • EEG (non-convulsive status epilepticus), VEP, EMG/NCVs
  • Brain MRI, MRA
  • Conventional angiogram (CNS vasculitis)
  • serum ammonium

CSF

  • 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

Blood/serum

  • 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

 

Biopsy

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

 

Reference:

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

Neurogenic Stress Cardiomyopathy

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.

 

hypothalamus-2-14-638.jpg

Figure-1-A-schematic-representation-of-the-hypothalamic-nuclei-and-the-distribution-of

*Paraventricular nucleus (PVN):   TRH release, CRH relesase, oxytocin release, vasopressin release, somatostatin release

**Dorsomedial nucleus (DMN): BP, HR, GI stimulation

 

Reference:

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.

Transphenoidal Cushing

Cushing’s disease:

 

Check labs:

  • AM cortisol and ACTH levels 6am and 6pm post-op day 1 and 2 (off steroids).

Treatment:

  • Avoid starting steroids until biochemical evidence of hypocortisolemia or clinical evidence of adrenal insufficiency.
  • Pt is deemed to be in early remission if morning cortisol level ≤5mcg/dl on postoperative day 1 or 2, necessitating glucocorticoid replacement.
  • Check BP q 2 hours. If BP<90/60 or nausea/vomiting/dizziness, immediately draw cortisol and ACTH levels and start Dexamethasone 0.5mg BID or HC 25mg daily (if on wards)
  • Assuming BP stable, start Dexamethasone 0.5 mg BID or HC 10mg AM and 5mg PM second post-op day 2
  • Send home on Dexamethasone 0.5 mg BID o HC 10mg AM and 5mg PM and have endocrinologist potentially adjust at 2 week post-op visit. Stress importance of this medication.
  • Subsequent assessments of corticotroph function are performed at a minimum of 3, 6, and 12 months after surgery. If successful surgery, unable to be weaned off of glucocorticoid replacement for at least 6-12 months after surgery.

 

ABCD2 Score

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TIA Prognosis and Key Mx Considerations by National Stroke Association

 

Reference:

Stroke.org. (2017). [online] Available at: http://www.stroke.org/sites/default/files/resources/tia-abcd2-tool.pdf?docID [Accessed 31 Jul. 2017].

Heads up Maneuver

Clinical scenario:  Patient with stroke comes in with large vessel occlusion and neuro deficits; he was placed supine for CT scan and NIHSS improved.  Vascular imaging still shows clot, but deficits are now nondisabling and NIHSS is low.  Should you proceed with thrombectomy?

Small study from UCLA used the Heads Up maneuver to select patients who should proceed to thrombectomy.

 

Patients included:

  1. stroke within 7.5h onset
  2. disabling neuro deficit on presentation
  3. improved while on CT to nondisabling deficit
  4. evidence (in MRA) of persisting large vessel occlusion

 

Heads up Maneuver: (performed in angio suite)

  1. position 90 degrees upright x 30 minutes, monitor BP/HR q5-10mins
  2. if worsened –> lower to supine, proceed with angio
  3. if remained stable –> lower to supine or 30 deg HOB; transfer to stroke unit

 

Pathophysiology of Delayed Collateral Failure:

STROKE –> increased CO / SVR –> improved flow to peri-infarct regions –> MI / CHF / dysrhythmias / sepsis / dysautonomia / drugs –> reduced CPP –> delayed collateral failure –> expansion of core infarct

 

Heads Up:

Head position influences collateral flow by increasing flow velocity in affected MCA. Impaired autoregulation allows perfusion to collateral channels to become passive-pressure dependent.  Head flat position increases CPP by 20%, improves neurologic function in 15% of patients.  Risk of aspiration PNA with head flat position is <5%.

 

Outcome:

The study found that heads up maneuver can be used to stress collateral systems and identify those patients who are vulnerable to hemodynamic failure.

  1. Only 5 patients included in the series – all had high NIHSS on arrival, improved during MRI scanning.
  2. Two patients tolerated 30 minutes, no thrombectomy performed, had excellent outcome with just medical therapy.
    1. *Spontaneous recanalization occurred within 72h (assumed that vigorous collaterals promoted recanalization).
  3. Three patients worsened with manuever and had successful recanalization and excellent outcomes as well.

 

Reference:

Ali, L., Weng, J., Starkman, S., Saver, J., Kim, D., Ovbiagele, B., Buck, B., Sanossian, N., Vespa, P., Bang, O., Jahan, R., Duckwiler, G., Viñuela, F. and Liebeskind, D. (2016). Heads Up! A Novel Provocative Maneuver to Guide Acute Ischemic Stroke Management. Interventional Neurology, 6(1-2), pp.8-15.

Mt. Fuji Sign

The Mt. Fuji sign is a radiologic finding seen in tension pneumocephalus.  Bilateral hypoattenuating collections are seen in the frontal subdural space, which causes compression and separation of the frontal lobes.

 

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Notice the widening of the interhemispheric space between the tips of the frontal lobes which resembles the silhouette of Mt. Fuji.  

 

In tension pneumocephalus, air enters into the cranial vault through disruption of the skull or skull base.  Air pressure increases within the subdural space due to a ball-valve mechanism, where air enters into subdural space but egress of air is blocked by an obstruction.

Tension pneumocephalus may occur after surgical evacuation of SDH (2.5-16%), skull base surgery, paranasal sinus surgery, posterior fossa surgery in sitting position, or head trauma.

To diagnose tension pneumocehpalus, CT findings should correlate with clinical signs of deterioration.

Peaking sign” (compression of frontal lobes without separation of frontal lobes) has also been linked to tension pneumocephalus.

Treatment includes:

  1. emergent decompression to alleviate pressure
    1. drilling burr holes
    2. craniotomy
    3. needle aspiration
    4. EVD placement
  2. administration of 100% oxygen
  3. closure of dural defects
  4. careful monitoring for clinical signs of deterioration
  5. serial CT scanning of brain

This is Mt. Fuji in Japan

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Reference

Michel, Steven J. “The Mount Fuji Sign.” Radiology 232.2 (2004): 449-450.

 

Upper Extremity Veins

Deep Veins:

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1. paired ulnar, radial and interosseous veins in forearm
2. paired brachial veins of upper arm
3. axillary vein (continues as subclavian vein)

 

Superficial Veins:

Upper_extremity_veins_edt

 

  1. cephalic vein
  2. basilic vein

 

References

“Deep Veins Of The Upper Extremity.” Uptodate.com. Web. 27 July 2017.

“Primary (Spontaneous) Upper Extremity Deep Vein Thrombosis.” Uptodate.com. 27 July 2017.