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Biomedical subjects

P Imesch

Publications and source records attributed to P Imesch.

6 recordsLinked to original sources
PubMed2005

[Intermittent diplopia after prolonged downward gaze to the right: what is the differential diagnosis?].

In general, intermittent diplopia evokes suspicion of ocular myasthenia gravis. However, other etiologies such as Brown syndrome or myokymia of the superior oblique may provoke intermittent diplopia. We present a case of intermittent diplopia due to a tumor in the cavernous sinus. A 59-year-old patient reported intermittent diplopia after prolonged downward gaze to the right. All other gaze directions failed to provoke symptoms. In 1992, the diagnosis of inactive macroadenoma of the pituitary gland was established and the patient underwent surgery and radiation therapy. At physical examination, prolonged downward gaze to the right of about 2 minutes provoked paresis of abduction, slight ptosis, and restriction of elevation on the left side, corresponding to sixth nerve palsy and palsy of the superior branch of the third nerve on the left side. MRI showed a relapse of the macroadenoma with infiltration of the cavernous sinus on the left side. The patient underwent surgery then focal radiation (gamma-knife). The clinical course was favourable and at the follow-up examination six months later, no diplopia was reported.

Abducens Nerve Diseases↗
PubMed2005

[Persistent visual problems thirty years after severe head trauma].

INTRODUCTION: Visual disturbances are common after severe head trauma. Some authors report 50 percent of these patients having damage to the visual system, ocular motor nerve palsies, or central eye movement disturbances. Visual disturbances influence prognosis and outcome of neurological rehabilitation, and, in most cases, diagnosis and treatment require interdisciplinary care. CASE REPORT: We report here a 50-year-old patient who suffered from severe head trauma at age 20. After coming out of a 4-week coma, he suffered visual disturbances such as blurred vision and diplopia. Visual acuity was 1.0 and the visual fields were intact. The symptoms remained unexplained for a long time. One year after the trauma, right trochlear palsy was diagnosed and surgical treatment was performed. However, the symptoms persisted, and one year later, a second operation was performed without changing the symptoms. During many years, prisms or refractive corrections were used to improve the visual disturbances, and finally, a psychiatric treatment was started. At age 40, the patient became presbyopic and his visual problems increased, especially for reading. When he was examined for the first time in our consultation, corrected visual acuity was 1.0 with a small hyperphoria of the right eye. During careful examination of the eye downgaze, a conjugate pure torsional nystagmus was observed, which disappeared in primary gaze position. CONCLUSION: Pure torsional nystagmus is difficult to diagnose, especially when it is provoked only by one gaze direction such as in our patient. As a sequel of the severe head trauma with brainstem contusion, this type of nystagmus is a rare form of central vestibular nystagmus, and may by modified by head rotation or suppressed by convergence. The "treatment" of the patient's blurred vision when reading was easy by ordering goggles with a near part placed near the primary gaze position and a 6 base down prismatic correction. Reading was then possible without provoking torsional nystagmus.

Coma↗
PubMed1998

[Varicella zoster virus and atypical necrotizing retinopathies in HIV and AIDS patients].

BACKGROUND: Necrotizing retinopathies of suspected viral origin, but which do not meet the criteria for either CMV-retinitis or acute retinal necrosis syndrome, have been grouped together under the term atypical necrotizing retinopathies. Nothing is known about their etiology. PATIENTS AND METHODS: Aqueous humor samples were drawn from two HIV-positive and eight patients with AIDS presenting with an atypical necrotizing retinopathy, additionally from six patients with acute retinal necrosis syndrome and 28 patients with active CMV-retinitis at the time of diagnosis as well as from thirty healthy controls at surgery. All samples underwent DNA extraction and amplification for viral DNA of HSV-1, VZV and CMV. RESULTS: VZV-DNA was detected in seven of nine aqueous humor samples derived from patients with atypical necrotizing retinopathies and in four of six samples from patients with acute retinal necrosis syndrome, but not in any one from the 28 patients with CMV retinitis. In the latter group, CMV DNA was detectable in 23 samples, in two of these additionally HSV-1 DNA. No viral DNA was amplified from any of the samples from healthy controls. CONCLUSIONS: Varicella zoster virus ist the leading cause of atypical necrotizing retinopathies. This should be considered in the antiviral chemotherapy. Moreover, we were able to establish the diagnosis using DNA amplification for the viruses of the herpes family irrespective of the etiology in 80% of necrotizing retinopathies.

AIDS-Related Opportunistic Infections↗
PubMed1997

The herpes simplex virus type 1 ribonucleotide reductase is required for acute retinal disease.

We have used a herpes simplex virus type 1 (HSV-1) ribonucleotide reductase (RR) null mutant (ICP6 delta) to determine if the HSV-1 RR is required for acute retinal disease. Injection of the ICP6 delta mutant into the vitreous induced mild transient signs of infection (vitreal infiltrate, retinal inflammation, and changes in retinal cytology). In contrast, the parental KOS and a revertant virus (ICP6 delta + 3.1) in which the RR gene had been restored, caused severe retinitis. Injection of media alone also induced mild transient signs of disease. Two months after infection, ICP6 delta injected eyes could not be distinguished from normal eyes. Repeated injection of ICP6 delta (3 times, 2 weeks apart) resulted in vitreal infiltrate near the site of injection but the retina did not appear damaged. The mutant, ICP6 delta, grew to peak titers 1 x 10(3) to 1 x 10(5)-fold lower and cleared faster than KOS or ICP6 delta + 3.1 in the injected eyes suggesting that the reduced virulence was due to reduced ability of the virus to grow. These results show that the viral RR is required for acute retinal disease.

Acute Disease↗
PubMed1996

Evaluation of a peptidomimetic ribonucleotide reductase inhibitor with a murine model of herpes simplex virus type 1 ocular disease.

The ribonucleotide reductase (RR) of herpes simplex virus type 1 (HSV-1) is an important virulence factor, being required for neurovirulence, ocular virulence, and reactivation from latency. The RR activity requires the association of two distinct homodimeric subunits, and the association of the subunits is inhibited in the presence of a peptide homologous to the carboxy terminus of the small subunit. A structural analog of the inhibitory peptide (BILD 1263) has been shown to inhibit the replication of HSV-1 at micromolar concentrations in vitro. We used a mouse model of HSV-1 ocular infection to determine the in vivo efficacy of topical BILD 1263. Treatment of HSV-1 KOS-infected mice resulted in significant reductions in the severity and incidence of stromal keratitis and corneal neovascularization. At higher concentrations (5%) BILD 1263 reduced the severity but not the incidence of blepharitis. Treatment with 5% BILD 1263 also reduced viral shedding from the cornea by 10- to 14-fold (P < 0.001). In uninfected mice treated with 5% BILD 1263, we found no evidence of corneal epithelial damage, conjunctivitis, or blepharitis, and histopathological studies revealed no changes in the corneas of these mice. These results show that the peptidomimetic RR inhibitor BILD 1263 is effective in preventing disease, has an antiviral effect in vivo, and has little or no toxicity.

Animals↗