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- Holmberg, Johan, et al.
(författare)
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Treatment of phobic postural vertigo A controlled study of cognitive-behavioral therapy and self-controlled desensitization.
- 2006
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Ingår i: Journal of Neurology. - : Springer Science and Business Media LLC. - 1432-1459 .- 0340-5354. ; 253:4, s. 500-506
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Tidskriftsartikel (refereegranskat)abstract
- In balance clinic practice, phobic postural vertigo is a term used to define a population with dizziness and avoidance behavior often as a consequence of a vestibular disorder. It has been described as the most common form of dizziness in middle aged patients in dizziness units. Anxiety disorders are common among patients with vestibular disorders. Cognitive-behavioral therapy is an effective treatment for anxiety disorders, and vestibular rehabilitation exercises are effective for vestibular disorders. This study compared the effect of additional cognitive-behavioral therapy for a population with phobic postural vertigo with the effect of self-administered vestibular rehabilitation exercises. 39 patients were recruited from a population referred for otoneurological investigation. Treatment effects were evaluated with the Dizziness Handicap Inventory, Vertigo Symptom Scale, Vertigo Handicap Questionnaire, and Hospital Anxiety and Depression Scale. All patients had a self treatment intervention based on education about the condition and recommendation of self exposure by vestibular rehabilitation exercises. Every second patient included was offered additional cognitive behavioral therapy. Fifteen patients with self treatment and 16 patients with cognitive-behavioral treatment completed the study. There was significantly larger effect in the group who received cognitive behavioral therapy than in the self treatment group in Vertigo Handicap Questionnaire and the Hospital Anxiety and Depression scale and its subscales. Cognitive-behavioral therapy has an additional effect as treatment for a population with phobic postural vertigo. A multidisciplinary approach including medical treatment, cognitive-behavioral therapy and physiotherapy is suggested.
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- Sköldenberg, Birgit, et al.
(författare)
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Incidence and pathogenesis of clinical relapse after herpes simplex encephalitis in adults.
- 2006
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Ingår i: Journal of neurology. - : Springer Science and Business Media LLC. - 0340-5354 .- 1432-1459. ; 253:2, s. 163-70
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVES: To study the occurrence of relapse of herpes simplex encephalitis (HSE) and to find out whether soluble activity markers in cerebrospinal fluid (CSF) indicate direct viral or immune- mediated events. METHODS: A consecutive series of 32 adult survivors of HSE were followed to determine the incidence of clinical relapse of HSE. Four patients had neurological deterioration interpreted as relapsing HSE. Four non-relapsing HSE cases were selected as matched controls. Fifty nine batched, paired CSF and serum samples from the eight HSE patients were analysed for soluble activity markers, predominantly cytokines and mediators (interferon-gamma, soluble CD8, tumour necrosis factor-alpha, and interleukin-10), amount of HSV-DNA and markers of glial and neuronal destruction (neurofilament protein, glial fibrillary acidic protein, S-100-beta, and neuron specific enolase). RESULTS: Relapse of HSE was diagnosed in 3 of 26 (12 %) acyclovir-treated patients (5 episodes during 6.1 years of followup) and in 1 of 6 vidarabine-recipients. All relapses occurred from 1 to 4 months after acute HSE, except for a second relapse after 3.3 years in one patient. Computer tomography at relapses revealed few abnormalities apart from those found during the primary disease. Intravenous acyclovir and corticosteroids were given for 7-21 days in all the relapse patients. All relapse patients seemed to recover to the pre-relapse condition. HSV-DNA was demonstrated in CSF in all patients during the acute stage but not in any of 13 CSF samples taken during relapse phases. The HSV viral load during the acute stage of HSE was not higher or of longer duration in the relapsing patients than in the non-relapsing HSE controls. The levels of sCD8 were increased in nearly all CSF samples tested with peaks of sCD8 at one month of acute HSE. In all episodes of relapse, sCD8 peaks were detected during the first week at high levels. CSF levels of neuron-specific enolase, S-100 and glial fibrillary acidic protein were markedly lower at relapse than at the acute stage of HSV-1 encephalitis. CONCLUSION: The lack of demonstrable HSV DNA in CSF, the lack of acute CSF signs and the lack of signs of neural and glia cells destruction indicate that a direct viral cytotoxicity is not the major pathogenic mechanism in relapse. Instead, the pronounced CSF proinflammatory immunological response and the relative lack of CSF anti-inflammatory cytokine IL-10 response suggest immunologically-mediated pathogenicity.
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