Provigil

By C. Kirk. California Lutheran University.

Treatment may be required for years to prevent relapses discount 100mg provigil fast delivery insomnia 2013. Ad Hoc Subcommittee of the American Academy of Neurology AIDS Task Force (1991) References Research criteria for diagnosis of chronic inflammatory demyelinating polyneuropathies (CIDP): report from the Ad Hoc Subcommittee of the American Academy of Neurology AIDS Task Force buy generic provigil 100 mg on-line . Neurology 41: 617–618 Hahn AF, Bolton CF, Zochodne D, et al (1996) Intravenous immunoglobulin in chronic inflammatory demyelinating polyneuropathy. A double blind placebo controlled, cross over study. Brain 119: 1067–1077 294 Hughes RA, Bensa S, Willison H, et al (2001) Randomized controlled trial of intravenous immunoglobulin versus oral prednisolone in chronic inflammatory polyradiculoneuropa- thy. Ann Neurol 50: 195–201 Kissel JT (2003) The treatment of chronic inflammatory demyelinating radiculoneuropathy. Semin Neurol 23: 169–180 Molenaar DSM, Vermeulen M, de Haan RJ (2002) Comparison of electrodiagnostic criteria for demyelination in patients with chronic inflammatory demyelinating polyneuropathy (CIDP). J Neurol 249: 400–403 Ropper A (2003) Current treatments for CIDP. Neurology 60 [Suppl] 3: S16–S22 295 Demyelinating neuropathy associated with anti-MAG antibodies Genetic testing NCV/EMG Laboratory Imaging Biopsy ++ ++ Demyelination occurs in sensory, and perhaps motor axons. Anatomy/distribution Symptoms of ascending numbness and ataxia progress slowly over months to Symptoms years. Intention tremor may develop late in Clinical syndrome/ disease. Cellular infiltration of nerves is minimal, compared to other inflammatory neuropathies. Laboratory: Diagnosis The availability of anti-MAG IgM antibody testing has made the diagnosis of the disorder much more common in recent times. Electrodiagnositic studies: Nerve conduction velocities are slowed, with no conduction block. Signs of motor dysfunction can be much more pronounced in EMG/NCV studies than the clinical picture would suggest. Strong cytotoxic drugs (cyclophosphamide, fludarabine) are medications that Therapy may slightly impact the course of the disease. Often, the patients that typically develop this neuropathy are elderly and cannot tolerate these treatments. Steroids, IVIG and plasma exchange are not effective. Recurrent therapy may be necessary, and usually patient response is poor, despite aggressive cytotoxic therapy. Prognosis Cocito D, Durelli L, Isoardo G (2003) Different clinical, electrophysiological and immuno- References logical features of CIDP associated with paraproteinemia. Acta Neurol Scand 108: 274–280 Eurelings M, Moons KG, Notermans NC, et al (2001) Neuropathy and IgM M-proteins: prognostic value of antibodies to MAG, SGPG, and sulfatide. Neurology 56: 228–233 Gorson KC, Ropper AH, Weinberg DH, et al (2001) Treatment experience in patients with anti-myelin-associated glycoprotein neuropathy. Muscle Nerve 24: 778–786 296 Miller-Fisher syndrome (MFS) Genetic testing NCV/EMG Laboratory Imaging Biopsy ++ ++ Anatomy/distribution Degeneration of axons and demyelination occurs, similar to AIDP. Symptoms Patients experience double vision, paresthesias, ataxia, and vertigo. In some cases, there is weakness of other motor cranial nerves and limbs. Clinical syndrome/ MFS is characterized by the triad of extraocular muscle weakness, ataxia, and signs areflexia. Pathogenesis MFS is considered a variant of AIDP, and cases initially appearing to fall in the classic MFS triad can progress to something more accurately diagnosed as AIDP. This condition is for some reason more common in Japan. It may be associated with Campylobacter jejuni (serotypes O–2 or O–10) or Haemophi- lus influenzae infections, but numerous other infections have been implicated.

T2-weighted MRI images reveal increased signal intensity in the basal ganglia and thalami discount 200 mg provigil free shipping insomnia diagnosis. Which of the following statements regarding this patient’s disease is true? The disease spreads primarily via the fecal-oral route B generic 100 mg provigil mastercard insomniac games. Neutrophilic CSF pleocytosis is distinctly unusual early in the course of this disease C. Using sentinel chickens to detect viral infection is important in con- trolling outbreaks E. The mortality from this disease is less than 20% E. The disease is caused by an arenavirus Key Concept/Objective: To be familiar with the presentation of an arboviral encephalitis and the means to detect the mosquito vectors Rapid alteration in mental status associated with fevers should raise suspicion for viral encephalitis. Of the various types of viral encephalitides, Eastern equine encephalitis (EEE), in a recent review, was found to have distinctive basal ganglion and thalamus involvement on MRI scan. It is one of the arboviral (arthropod-borne) encephalitides and is spread by mosquito bite rather than a fecal-oral route. Neutrophilic CSF pleocytosis would not be unusual early in the course of any acute viral CNS infection and is common in EEE. Control of outbreaks comes from monitoring and controlling the mosquito vectors. Presence of the virus in swampy habitats can be detect- ed by recovering virus from mosquitoes or by measuring serum antibodies in wild passer- ine birds or caged sentinel birds (chickens). The are- naviruses are endemic in rodents, with lymphocytic choriomeningitis virus being most common in the United States. A 59-year-old woman from Missouri has a 20-year history of systemic lupus erythematosus, for which she is taking corticosteroids. One day before admission, the patient started taking ibuprofen for a flare in arthralgias. Chest x-ray, complete blood count, and urinalysis are normal. CSF analysis shows 400 WBC/mm3, with 51% monocytes, normal glucose, slightly elevated protein, and negative Gram stain for bacteria. Without therapy, she becomes fully alert and afebrile within 24 hours. At this point, she relates that she had two identical episodes within the past 5 years, each after ibuprofen use. Systemic lupus erythematosus cerebritis 50 BOARD REVIEW C. Louis encephalitis Key Concept/Objective: To be aware that both infectious and noninfectious processes can present as an aseptic meningitis or meningoencephalitis syndrome The patient has evidence of CNS inflammation with a mononuclear CSF pleocytosis. Enteroviruses commonly cause acute viral meningitis, but recurrent acute infections would be very unlikely. Louis encephalitis—the other “SLE”—is an arboviral encephali- tis that would neither resolve clinically within 24 hours nor recur. Mollaret recurrent meningitis might have a herpesvirus origin, but there is a more likely explanation in this patient. Cerebritis can be part of active systemic lupus erythematosus, but rapid resolution and no other manifestations of active disease argue against the diagnosis. Nonsteroidal anti-inflammatory drugs can cause a meningoencephalitis, especially in patients with underlying collagen vascular diseases. Three identical episodes occurring immediately after the use of ibuprofen, with rapid improvement after its removal, argue for this diag- nosis. Eight weeks ago, a 26-year-old woman with Hodgkin disease developed a zosteriform eruption of the left periorbital and left forehead regions. The skin lesions resolved, and apart from episodic neuralgic pains, the patient was doing well until today, when she experienced the sudden development of right hemi- plegia. On examination, the patient is awake, afebrile, and aphasic; residual small scabs are noted on the left side of the face, and she has a dense right hemiplegia. For this patient, which of the following diagnostic test results is most likely? Increased left frontal and temporal lobe intensity on T2-weighted MRI scan images B.