1. Effect of cilostazol in patients with aneurysmal subarachnoid hemorrhage: A systematic review and meta-analysis.
Niu et al {J Neurol Sci, 2014}
"Two randomized controlled trials and two quasi-randomized controlled trials with a total of 340 patients were included. The incidence of symptomatic vasospasm (RR=0.47; 95% CI, 0.31-0.72; p<0.001), severe vasospasm (RR=0.48; 95% CI, 0.28-0.82; p=0.007), vasospasm-related new cerebral infarctions (RR=0.38; 95% CI, 0.22-0.67; p=0.001), and poor outcome (RR=0.57; 95% CI, 0.37-0.88; p=0.011) were significantly lower in the cilostazol group. The numbers needed to treat for these outcomes were 6.4, 6.3, 5.7, and 5.4, respectively. Mortality rate differences between the two groups were insignificant. No statistical heterogeneity was found for all outcomes. These results show that cilostazol can decrease the incidence of symptomatic vasospasm, severe vasospasm, vasospasm-related new cerebral infarctions, and poor outcome in patients with aneurysmal SAH."

2. Effects of cilostazol on cerebral vasospasm after aneurysmal subarachnoid hemorrhage: a multicenter prospective, randomized, open-label blinded end point trial.

Senbokuya et al {JNS}
"Cilostazol, a selective inhibitor of phosphodiesterase 3, may attenuate cerebral vasospasm because of its antiplatelet and vasodilatory effects. A multicenter prospective randomized trial was conducted to investigate the effect of cilostazol on cerebral vasospasm."
Inclusion criteria: Patients in Japan admitted with SAH caused by a ruptured anterior circulation aneurysm who were in Hunt and Kosnik Grades I to IV and were treated by clipping within 72 hours of SAH. Nov 2009 to Dec 2010
Comparison: usual therapy group (control group) vs add-on 100 mg cilostazol twice daily group (cilostazol group).
End points: onset of symptomatic vasospasm (primary), onset of angiographic vasospasm, new cerebral infarctions related to cerebral vasospasm, clinical outcome (mod rankin scale), and length of hospitalization.
Results: N=109
Symptomatic vasospasm occurred in 13% (n = 7) of the cilostazol group and in 40% (n = 22) of the control group (p = 0.0021).
The incidence of angiographic vasospasm was significantly lower in the cilostazol group than in the control group (50% vs 77%; p = 0.0055)
Multiple logistic analyses demonstrated that nonuse of cilostazol is an independent factor for symptomatic and angiographic vasospasm.
The incidence of new cerebral infarctions was also significantly lower in the cilostazol group than in the control group (11% vs 29%; p = 0.0304,).
Clinical outcomes at 1, 3, and 6 months after SAH in the cilostazol group were better than those in the control group, although a significant difference was not shown. There was also no significant difference in the length of hospitalization between the groups. No severe adverse event occurred during the study period.
3. Triple H therapy for SAH: hypertension, hypervolemia, hemodilution. Although hypertension may be the only one of these things that work, and additionally, hemodilution may counteract or worsen the benefit of hypertension in decreasing O2-carrying capacity of blood.
4. Hemodynamic management of subarachnoid hemorrhage.
Treggiari MM1; Participants in the International Multi-disciplinary Consensus Conference on the Critical Care Management of Subarachnoid Hemorrhage. {Neurocrit Care. 2011}
-Literature review (years 2000-2010) on hemodynamic augmentation therapies in patients with subarachnoid hemorrhage. Among the eligible reports identified, 11 addressed volume expansion, 10 blood pressure management, 4 inotropic therapy, and 12 hemodynamic augmentation in patients with unsecured aneurysms.
-Hypervolemia did not appear to confer additional benefits over normovolemic therapy, with an excess of side effects occurring in patients treated with hypervolemic targets.
-Hypertension was associated with higher cerebral blood flow, regardless of volume status, with neurological symptom reversal seen in two-thirds of treated patients.
-Limited data were available for evaluating inotropic agents or hemodynamic augmentation in patients with additional unsecured aneurysms. In the context of sparse data, no incremental risk of aneurysmal rupture has been reported with the induction of hemodynamic augmentation.
5. Effect of different components of triple-H therapy on cerebral perfusion in patients with aneurysmal subarachnoid haemorrhage: a systematic review.
Dankbaar JW et al {Crit Care 2010}
-Systematic literature review (until 2009, excluding case reports) on the effect of triple-H components on cerebral perfusion in SAH patients.
-Outcome: cerebral blood flow (CBF in ml/100 g/min).
-11 studies (4-51 patients per study) were included (one randomized trial).
-Hemodilution did not change CBF.
-One of seven studies on hypervolemia showed statistically significant CBF increase compared to baseline; there was no comparable control group.
-Two of four studies applying hypertension and one of two applying triple-H showed significant CBF increase, none used a control group.
-There is no good evidence from controlled studies for a positive effect of triple-H or its separate components on CBF in SAH patients. In uncontrolled studies, hypertension seems to be more effective in increasing CBF than hemodilution or hypervolemia.

6. The evolving role of hemodilution in treatment of cerebral vasospasm: a historical perspective.

Chittiboina P et al {World Neurosurg. 2011}
-Literature review on hemodilution as a therapeutic modality in treatment of cerebral vasospasm.
-Evidence has been accumulating against the efficacy of HHH therapy and hemodilution in particular.
-Although HHH therapy and consequently hemodilution has wide support, the evidence for its effectiveness remains equivocal.
-At the time of this study, the burden of evidence appears to be tipped away from hemodilution as a therapeutic modality.
7. Standard workup in a young or middle aged woman who presents with lower abdominal pain:
-Pregnancy test
-GC/chlamydia
-Wet mount
-Urine dipstick
-Pelvic & abdominal exam.
8. Back pain descriptors and suggested diagnoses
-Pain worse with movement and sitting is suggestive of a mechanical cause of back pain, such as a lumbar strain, disc herniation, or degenerative arthritis.
-Pain radiating down the leg and numbness indicate nerve involvement, such as in disc herniation.
-Pain that improves with the supine position suggests spinal stenosis and disc herniation.
-Dull, throbbing pain that progresses slowly, and increases with recumbency or cough in an older patient with a history of cancer, malignancy is likely
-Aching back and posterior thigh discomfort that increases with activity or bending- think spondylolisthesis
9. Overview: physical exam for back pain: 
1. Look at posture, contour and symmetry (lordosis, kyphosis, scoliosis)
2. Palpate for any tenderness, tightness, rope-like tension, or inflammation in the paraspinous muscles or tenderness over bony prominences. This checks for muscle spasm, vertebral fracture, or infection. Point tenderness is suggestive of fracture, infection, malignancy.
3. Range of Motion:
-Lumbar Flexion (normal is 90 degrees): Best measure of spine mobility. Restriction and pain during flexion are suggestive of herniation, osteoarthritis, or muscle spasm.
-Lumbar Extension (normal is 15 degrees): Pain with extension is suggestive of degenerative disease or spinal stenosis.
-Lateral motion (normal is 45 degrees): Most patients should be able to touch the proximal fibular head of the knee. Pain on the same side as bending is suggestive of bone pathology (osteoarthritis or neural compression). Pain on the opposite side of bending is suggestive of a muscle strain.
4. Gait: Heels and toe walk. Expect normal gait, even with disc herniation.
-Difficulty with heel walk is associated with L5 disc herniation
-Difficulty with toe walk is associated with S1 disc herniation
-Have the patient go from a standing to squatting position: With central spinal stenosis, squatting will reduce the pain.
5. DTR:
-0: none, 1: reduced, 2. normal, 3: hyperreflexive, 4: clonus
-Patella is L3/L4, Achilles is L4/L5. Reduced reflexes implies pathology at those respective levels
-Increased reflexes supports UMN disease, like spinal stenosis
6. Strength
-0: none, 1: flicker, not enough to move limb, 2: move limb, not against gravity, 3: move limb against gravity, no resistance 4: some resistance, 5: normal strength.
-Iliopsoas/Hip Flexion (L 2, 3, 4)
-Quads/Knee Extension (L 2, 3, 4)
-Hip Adduction (L 2, 3, 4)
-Hip Abduction (L 4, 5, S1)
-Ankle Dorsiflexion/Tibialis Anterior (L 4, 5)
-Great toe Dosriflexion/Extensor hallucis longus (L5... L4?)
-Knee Flexion/Hamstrings (L 5, S1, S2)
-Ankle Plantar Flexion/Gastrocnemius (S 1, S 2)
10. Focused neuro exam for lower back pain: 
-Check the patellar and Achilles reflexes.
-Check muscle strength for hip flexion, abduction, and adduction; knee extension and flexion; ankle dorsiflexion and plantar flexion.
-Test for sharp and light touch along the dermatomal distribution of the great toe (L5), lateral malleolus and posterolateral foot (S1).