• Xanthochromia is the yellowish discoloration of the supernatant from centrifuged cerebrospinal fluid (CSF).

• Xanthochromia is an abnormal finding and results from the lysis of red blood cells.

• Xanthochromia is present is CSF in > 90% of patients within 12 hours of subarachnoid hemorrhage (SAH) onset.

• Several conditions cause increased intracranial pressure (ICP), requiring lumbar puncture (LP) with opening pressure (OP) measurement for diagnostic and therapeutic management.

• Examples of such include:  pseudotumor cerebri, (cryptococcal) meningitis, intracranial mass, and intracranial hemorrhage.

• In order to ensure an accurate measurement, OP should be assessed while the patient is in the lateral decubitus position with the neck and legs in a neutral position.

• Normal OP ranges from 10 to 100 mm H₂0 in children, 60 to 200 mm H₂0 after age 8, and up to 250 mm H₂0 in the obese.  OP > 250 = intracranial hypertension.

• OP (the meniscus level) can fluctuate by 2 to 5 mm H20 with patient's pulse and by 4 to 10 mm H20 with patient's respirations.

• A patient's symptoms of headache and/or neurologic deficit is often relieved by lowering the ICP through slow removal of CSF during LP.  The pressure level should not be lowered by any more than 50% of the initial OP.

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• 5 to 10% of TIA victims go on to have a complete stroke within 7 days.

• The following validated ABCD clinical prediction rule can be used to risk stratify your next TIA patient in determining who requires an expedited in-patient work-up:

          Risk Factor                                                                        Score

• Age > or = 60                                                                      1

• Blood Pressure (SBP > 140 and/or DBP > or = 90)                    1

• Clinical Features (choose one)

          -- Unilateral weakness                                                           2

          -- Speech impairment w/o weakness                                       1

          -- Other                                                                               0       

• Duration of Symptoms (minutes)

          -- > 60                                                                                2

          -- 10 to 59                                                                           1

          -- < 10                                                                                0

                                                                                              Total 0-6

	Seven-day risk of stroke (stroke/no. of patients; %)
Point total	Possible TIA*	Probable or definite TIA
0 or 1	0/28 (0)	0/2 (0)
2	0/74 (0)	0/28 (0)
3	0/82 (0)	0/32 (0)
4	1/90 (1; 95% CI, 0 to 3)	1/46 (2; 95% CI, 0 to 6)
5	8/66 (12; 95% CI, 4 to 20)	8/49 (16; 95% CI, 6 to 27)
6	11/35 (31; 95% CI, 16 to 47)	11/31 (35; 95% CI, 19 to 52)
Total	20/375 (5.3; 95% CI, 3 to 7.5)	20/188 (10.6; 95% CI, 6 to 15)

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• Patients who have recently undergone aneurysmal coiling commonly present to the ED with complaints of new or worsened focal neurologic deficits that may be suggestive of stroke.

• Aneurysms can be stabilized by clipping or coiling them.  Coiling is performed in a minimally invasive manner, wherein platinum (a material that can be visualized radiographically and is flexible) coils are deployed into the bulb of the aneurysm, via femoral artery cannulation.

• The relative risk of mortality or morbidity at one year post-coiling was found to be 22.6% less than that associated with clipping.  The latter is an older, more invasive technique requiring craniotomy and direct manipulation of the brain.

• Hemorrhage is a less likely complication related to aneurysm coiling, thus your indication for a non-contrast Head CT in these patients would most appropriately be "rule out infarct" rather than "rule out bleed." 

• Brain infarct is the more common complication of this treatment, and results from the accidental embolization of plaque during the coiling procedure.

• Here are a couple of great links with illustrated overviews of the process of coiling, including a real time You Tube clip:
  
  http://www.brainaneurysm.com/aneurysm-treatment.html
  
  http://www.youtube.com/watch?v=Mvy8g_oDbbk

• Syncope is defined as a transient loss of consciousness and accounts for an estimated 1% to 3% of emergency department (ED) visits.
   
• While syncope typically is of benign origin, it occasionally signals significant mortality and morbidity, which can make determining the disposition of syncope patients a challenge.
   
• The San Francisco Syncope Rule (96% sensitivity, 62% specificity) is a clinical tool used to determine which syncope patients are at low risk for a short-term (7-day) serious outcome (i.e. MI, arrhythmia, PE,  stroke, SAH, significant hemorrhage, any condition causing or likely to cause a return ED visit or hospitalization).
  Specifically, absence of all of the following 5 findings (acronym CHESS) were associated with no serious outcome within 7 days of the syncopal episode according to this rule:
  • Congestive heart failure
  • Hematocrit less than 30
  • EKG Abnormalities
  • Systolic BP less than 90
  • Shortness of breath
     
• While this decision rule, in addition to one's clinical skill, may be used as a guide in caring for and dispositioning syncopal patients, know that its ability to be extrapolated to a general population of ED patients has yet to be validated.

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• The majority of those afflicted with bell palsy experience neurapraxia or a local nerve conduction block, which usually predicts a prompt and full recovery.  80% to 90% of Bell Palsy patients experience recovery without any noticeable disfigurement within 6 weeks to 3 months.

• Some Bell Palsy patients experience axonotmesis, disruption of the axons, which increases their risk of an incomplete recovery.

• One is at higher risk of developing sequelae in the following scenarios: 

          --  Age greater than 60 years

          --  Diabetes

          --  Decreased taste or salivary flow on the affected side

          --  Complete paralysis

• Common post-Bell Palsy sequelae that you may see clinically include:

          --  Synkinesis - abnormal contracture of facial muscles with smiling or

               closing eyes; may cause slight chin movement with blinking, eye closure

               with smiling, contracture around mouth with blinking.

          --  Crocodile tears - lacrimation while eating.

          --  Hemifacial muscle spasms - tonic contractures of affected side of face, 

               rare, often seen during times of fatigue, stress, or while sleeping.

• Bell Palsy is the most common cause of unilateral facial weakness.

• It is caused by edema and ischemia causing compression of the facial nerve (cranial nerve seven).

• While Bell Palsy is by definition an idiopathic facial palsy, the etiology is often infact discovered and attributed to conditions such as Lyme Disease, Herpes Simplex Virus, and HIV.

• Classic symptoms of Bell Palsy include:

          -- acute onset of unilateral upper and lower facial paralysis (over 48 hr. period)

          -- posterior auricular pain

          -- decreased tearing

          -- hyperacusis (due to stapedius muscle weakness)

          -- taste disturbances

• Bell Palsy is a diagnosis of exclusion.  If the facial paralysis is isolated to the lower face, if there is associated contralateral weakness, and/or if there is diplopia, a central cause for the symptoms, rather than Bell Palsy, must be strongly considered.

• Neurologic complications affect 30 to 60% of allograft organ transplant recipients.
   
• Many of these complications are related to immunosuppresant medication neurotoxicity.
   
• Calcineurin inhibitors such as tacrolimus (FK-506 or Fujimycin) and cyclosporin are classically associated with the following neurologic disorders:
  • Cranial Nerve Palsy:  Tacrolimus toxicity can cause reversible  internuclear ophthalmoplegia.
  • Movement Disorders:  Tacrolimus and cyclosporin often cause tremor, which can be further compounded by the development of asterixis should the patient also have significant renal or hepatic insufficiency.
  • Visual Abnormalities:  Cortical blindness, visual disturbances, hallucinations, retinal toxicity, and optic neuropathies have all been attributed to calcineurin inhibitor toxicity.  Opsoclonus (rapid, involuntary, uncontrolled, multivectorial eye movements) has specifically been associated with cyclosporin neurotoxicity. 
     

• Neurotoxicity related to immunosuppresant drug therapy is most likely to occur early after transplantation and during a rejection episodes, times at which medication doses are typically at their highest.  Dose adjustment often results in resolution of symptoms.
   
• Be sure to check drug levels of immunosuppresant medications, particularly when a transplant patient presents with a neurologic disorders.

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