(no subject)

http://www.wimp.com/newdevice/

Papilledema and obstructive sleep apnea syndrome.

Purvin VA, Kawasaki A, Yee RD.

 Abstract

OBJECTIVES:

To characterize the pathogenesis and clinical features of optic disc edema associated with obstructive sleep apnea syndrome (SAS).

METHODS:

A series of 4 patients with SAS and papilledema (PE) underwent complete neuro-ophthalmologic evaluation and lumbar puncture. In 1 patient, continuous 24-hour intracranial pressure (ICP) monitoring was also performed.

RESULTS:

All 4 patients had bilateral PE that was asymmetric in 2. Three patients had optic nerve dysfunction, asymmetric in 1, unilateral in 2. Daytime cerebrospinal fluid pressure measurements were within normal range. Nocturnal monitoring performed in one patient, however, demonstrated repeated episodes of marked ICP elevation associated with apnea and arterial oxygen desaturation.

CONCLUSIONS:

We propose that PE in SAS is due to episodic nocturnal hypoxemia and hypercarbia resulting in increased ICP secondary to cerebral vasodilation. In these individuals, intermittent ICP elevation is sufficient to cause persistent disc edema. These patients may be at increased risk for developing visual loss secondary to PE compared with patients with obesity-related pseudotumor cerebri because of associated hypoxemia. The diagnosis of SAS PE may not be appreciated because daytime cerebrospinal fluid pressure measurements are normal and because patients tend to present with visual loss rather than with symptoms of increased ICP.

Common pitfalls in management IIH

Management Errors:
missing venous sinus thrombosis
failure to address other secondary causes (e.g., anemia, hypoxia)
relying on optic disc appearance without monitoring visual fields
being too slow to proceed to surgical intervention

Papilledema pearls

 

1. Cotton wool spots OFF disk may suggest hypertensive syndrome

 

2.  Hemorrhages off disc suggest central retinal vein occlusion

 

3.  New onset pulsatile tinnitus is significant finding indicating need to look for increased ICP, as well as transient obscurations, graying of vision for twenty seconds, with postural change and headache.  Field before acuity is affected, disc edema usually affected.

 

4.  MRI findings  may include disc enhancement, occassionally, enhanced perioptic space (40 %), flattening of posterior globe (80 %), empty sella  Get MRI/MRV

 

5.  Check blood pressure

 

6.  Blood:  CBC, electrolytes for Addison's, Ca for HPT, ANA for lupus that is it..  Lumbar puncture always.

 

7.  Must check visual fields  since acuity is preserved. That is affected early.

 

8.  Protect optic nerve function and appearance: the two goals of management of pappilledema, not normal pressure, that is not a goal.

 

9.  Therapy:  diamox 500 bid to start, add Lasix 40  mg q am with Kcl 20 meq.

 

10. Fenestration protects eye, but does not lower headache or pressure.  Consider fenestrating patients with progressive visual loss, severe loss early, patients with severe papilledema at risk for hypotension (dialysis) or patients unable to comply with monitoring vision.  Shunt is a better treatment for headache of IIH.

 

 

h't Valerie Purvin AAN 2013

Causes of pappilledema (bilateral) with good optic nerve function

 

increased intracranial pressure

 

malignant hypertension

 

toxins (amiodarone,cyclosporine)

 

sleep apnea syndrome

 

uveitis, eg. sarcoidosis

 

 

Fwd: Neurological complications of influenza

Neurological complications of influenza

Tsai JP, Baker AJ.  Neurocritical Care 18:2013; 118-130 (review article)

There are five types of encephalopathy, two benign and three malignant.  Typically they occur a mean of two weeks post influenza, and are not associated with CNS inflammation.  They include:

1)  MERS (mild encephalopathy with reversible splenial lesion)-   influenza symptoms, then prodrome of decreased level of consciousness, seizures, CSF pleocytosis, EEG abnormal, often within 103 days, and total resolution within one month with or without therapy.  Agents include infl A and B, Legionella, Staph and Strep species,  and E Coli.  Splenial lesion is thought to represent intramyelinc edema with fiber separation.

2)  HSES (hemorrhagic shock and encephalopathy syndrome (peds only)) shock, seizures, coma, DIC, diarrhea, drop HB/platelets, elevated LFT's, renal dysfunction, acidoses, negative blood and CSF cultures.  "Definite" all 9 criteria are met, "probably" is 7-8 criteria met.  Originally defined by Levin et al, 1982.  Biphasic course with improvement then deterioration may occur.  Abnormal EEG, diffuse cerebral edema, hemorrhagic necrosis occur.  Morbidity  plusmortality may > 90 percent.

3) ANE-- Acute necrotizing encephalopathy (pediatric and adults)-- most common complication of influenza.  Course is fever, URI prodrome, then rapid and severe decline in consciousness often with seizures at onset and within 1-3 days of onset of systemic symptoms.  CSF shows mild pleocytosis, limited utility.  MRI shows severe symmetric, diffusion restricting lesions in both thalami, rostral midbrain tegmentum, putamena, periventricular white matter and cerebellar hemispheres.  Decreased flow without stenosis or emboli is seen in thalamaperforators, SCA's , and deep internal and great cerebral veins.  Early steroid therapy aids survival among patients without brainstem lesions. 

4)  (AESD) Acute encephalopathy with seizures and late restricted diffusion-- predominantly a pediatric diagnosis with variable features and prognosis and several eponyms

Pearls on carotid cavernous fistulas

from Wijdicks text on acute neurology

1.  Associations--
      remote trauma
      post transsphenoidal surgery
      post ethmoidal surgery
     post carotid surgery
     Ehlers Danlos syndrome
     pregnancy

2.  Visual loss is due to increased intraocular pressure or reverse of flow or thrombus in superior opthalmic vein (SOV).  Balloon or coil occlusion has been reported (sometimes) to reverse blindness

3.  On angiography, immediate opacification of carotid sinus is seen after carotid injection.

4.Clinical findings include III n palsy, lid swelling, tortuous veins, dis edema and visual loss.

tests to consider in patients with encephalitis

serology- HIV, EBV, acute and convalescent phases St Louis encephalitis, eastern equine encephalitis, LaCrosse and West Nile viruses; acute and convalescent phase serum titers of myc. pneum, ricketsii ricketsiae, ehrlichia chaffensis, anaplasma phagocytophilum; rpr and fta;  lyme (ELISA and Western blot), IgG for toxoplasma; serum cryptococcal antigen; complement fixing or immunodiffusion antibodies for coccidio species

blood cultures;

Respiratory secretions pcr for myc. pneum;

CSF cultures;  IgM for St Louis, West Nile and VZV; vdrl and fta, IgG index, lyme (elisa and Western blot), CSF cryptococcal antigen; CSF histoplasma antigen;  complement fixing or immunodiffusion antibodies for coccidio species

CSF pcr's for HSVE I and II, enteroviruses, VZV, EBV, ehrlichia and anaplasma species, myco. pneum.

blood smears for morulae

culture respiratory secretions,nasopharyx, throat and stool

skin culture of rash if present for HSV and VZV

urine -- histoplasma antigen

Signs indicating causes in confused febrile patients

from  Wijdicks, The practice of emergency and critical care neurology.

Rash-- ricketsiae, aspergillus, vasculitis

petechiae-- TTP, meningococcemia, endocarditis, drug eruption, leukemia

splenomegaly-- toxo, TB, sepsis, HIV, lymphoma

pulmonary infiltrates-- legionella, fungi, TB, mycoplasma, pneumonia, tick borne, Q fever

Meningococcal meningitis and corticosteroids

Brust JCM.  Meningococcal meningitis, dexamethasone and Class III evidence(editorial) Neurology 2012; 79: 1528-9.

The most recent Cochran review shows a benefit of adjunctive dexamthasone to mortality in Streptococcalbut not N meningitidis meningitis with benefits to adults and children in high but not low income countries ( See Brouwer MC et al, 2010).  Significantly, however, dexamethasone does no harm.  Recommendation is .6 mg/kg.day for four days.  It should be given prior to or with the first dose of antibiotic before lysis occurs.  In practice, steroids rarely are stopped when Neiss men is identified as the organism, but that does not harm the patient.

Postural tachycardia syndrome (POTS)

A heterogenous and multifactorial disorder.

Benarroach EE, Mayo Clin Proc 2012; 87:(12) 1214-1225.

A recent review article by the amazing Eduardo Benarroch. 

Definition POTS:  (IN ADULTS) HR increase of 30 bpm within 10 minutes of standing or head up tilt (HUT) without orthostatic hypotension.  Definition may be inadequate for yong teens or those with low resting HR.  Lesser degrees of abnormality is called "orthostatic intolerance."

Symptoms: of cerebral hypoperfuson and (reflex) sympathetic hyperactivity relieved by incumbency.  They include, light headedness, blurred vision, cognitive difficulty, generalized weakness (for hypoperfusion) and palpitations, chest pain, tremulousness (for sympathetic part).   One third have secondary vasovagal syncope with typical exacerbating factors (heat exposure, heavy meals, exertion, prolonged incumbency, menses and certain drugs).

Demography:  females have more (4.5:1), age usually 15-25, half have preceding viral illness and 25 % have a positive family history of.Deconditioning, psychological factors are important and autonomic defined abnormalities are relatively uncommon. 

Pearls:
1.  "Neuropathic" POTS is a subtype with LE sympathetic denervation with loss of sweating, quantitative sudomotor testing, impaired NE release in LE's in response to orthostatic stress. Its probably due to inpaired vasoconstriction and venous pooling in legs. They are also the high flow subtype in blood flow testing of legs. 14 % have ganglionic acetylecholine receptor antibody, hence may be autoimmune/

2.  Hyperadrenergic POTS-- 30-40 % have high NE levels (>600 pg/mL), HTN during HUT, tachycardia, HTN and hyperhidrosis episodes triggered by orthostasis OR emotional stimuli/physical activity.  This is low volume group with supine vasoconstiction, supine tachycardia, pale and cold skins.  Hyperadrenergic state due to norepinephrine transporter (NET) blockade by drugs (TCA's. methylphenidate and related stimulants and others) or secondary to mast cell disorders.  Consider hyperthyroidism or pheochromocytoma in these patients. 

3.  Hypovolemic POTS (28 %).  May be due to low renin/aldosterone secretion or to inappropriately high ACE-2 activity.  May be related to primary GI disorder of N/V/D. 

4. Comorbidities:  Visceral pain and dysmotility, CFS, FM, sleep disorders, myofascial pain, Ehler Danlos syndrome especially type III with variations in tenascin X.  May be related to early onset of chronic pain, with anxiety and sensory amplification state.  Headache with or without CSF leak.