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T Büttner

Publications and source records attributed to T Büttner.

69 records · Page 4Linked to original sources
PubMed1993

Disturbance of colour perception in Parkinson's disease.

A computer-aided method for the determination of colour fusion time (CFT) was developed. CFT indicates the acuity of the perception of monochromatic contours. CFT was determined in 36 patients with Parkinson's disease (PD) and compared with a group of 36 age- and sex-matched controls. Patients with PD generally had a shortened fusion time, especially for dark-green, light-blue and dark-red stimuli. The results give evidence to the hypothesis of a colour perception disorder in PD. The physiological and pathoanatomical basis of this phenomenon is unknown, but a functional deficit of cortical neurons may be a probable cause.

Adult↗
PubMed1993

[Topodiagnosis of Creutzfeldt-Jakob disease using HMPAO-SPECT].

An 80-year old female presented with early stage Creutzfeldt-Jakob disease with clinical, neurophysiological and neuropathological findings suggesting a focal involvement of the brain. HMPAO SPECT disclosed asymmetries of regional cerebral perfusion, thus suggesting that it may be a further diagnostic instrument in this disease.

Aged↗
PubMed1993

[Cerebral vasculitis in Crohn disease].

Central nervous system vasculitis in Crohn's disease. A 36-years old man was referred to the hospital because of severe headache, vertigo and right sided combined motor-sensory hemiparesis. There was a history of Crohn's disease with an acute exacerbation only two months ago. Magnetic resonance imaging detected a vascular lesion of the left brainstem and serologic investigations revealed circulating immunocomplexes and p-antineutrophil cytoplasmic autoantibodies (p-ANCA). Further investigations care no evidence of arteriosclerotic cerebrovascular disease. These findings therefore suggest that cerebral vasculitis secondary to Crohn's disease was the underlying cause of this focal neurologic deficit.

Adult↗
PubMed1992

Long-term prognosis of infratentorial transient ischemic attacks and minor strokes.

BACKGROUND AND PURPOSE: This study was performed to gather information about long-term prognosis after infratentorial transient ischemic attacks and minor strokes and about the factors influencing it. METHODS: We included 226 patients with transient ischemia and 169 patients with a minor stroke of the brain stem/cerebellum consecutively admitted to a neurological department. Medical records and the findings of computed tomography, Doppler ultrasonography, and angiography were evaluated retrospectively. Follow-up information was gathered from the patients and their physicians by questionnaires. Complete follow-up information was available for 381 patients. RESULTS: During a mean follow-up of 3.9 years, 15.7% of the 381 patients suffered a stroke and 6.8% a myocardial infarction; 15% died. Kaplan-Meier estimates revealed a cumulative stroke rate of 5.1% within the first year and a risk of stroke, myocardial infarction, or death of any cause of 9.8%. In a proportional hazards model, the time-dependent risk of stroke was significantly increased by increasing age (p = 0.018), minor stroke (p = 0.0005), hypertension (p = 0.022), previous stroke (p = 0.0006), and carotid artery occlusive disease (p = 0.0065). The probability of stroke, myocardial infarction, or death was influenced by age (p = 0.0001), minor stroke (p = 0.006), diabetes (p = 0.015), previous stroke (p = 0.002), infarct on a computed tomogram (p = 0.041), and carotid artery disease (p = 0.032). CONCLUSIONS: Long-term prognosis after brain stem/cerebellar transient ischemic attacks and minor strokes is significantly influenced by age, diabetes, hypertension, previous stroke, and concomitant carotid artery disease. Patients with transient ischemic attacks have a better prognosis than those with minor stroke.

Cerebellum↗
PubMed1991

[Thalamic infarcts--clinical aspects, neuropsychological findings, prognosis].

Results of clinical investigations and CCT of 23 patients with thalamic infarctions were evaluated retrospectively. Nineteen patients underwent a clinical and 15 a neuropsychological examination one to 5 years after their stroke. Regarding the affected vascular territory, the patients were divided into the following subgroups: paramedian infarctions (posterior thalamo-subthalamic arteries, 13 patients, among them 5 bilateral infarcts); anterolateral infarcts (tuberothalamic arteries, 5 patients); posterolateral infarcts (thalamo-geniculate arteries, 5 patients). The leading symptoms of paramedian thalamic infarcts were disturbance of consciousness, amnesia and vertical gaze palsy. The patients with anterolateral thalamic infarctions became acutely confused and disorientated, whereas those with posterolateral infarcts suffered from focal neurological deficits in the first place. Five patients with leftsided thalamic infarctions of varying localization were aphasic. Two patients died within the observation period. A slight hemiparesis was detected in two patients and a vertical gaze palsy in 4, respectively, by the neurological reexamination one to 5 years after the stroke, whereas the clinical findings in 11 patients were completely normal. However 5 patients had a chronic psychosyndrome. The neuropsychological examination showed in some cases disorders of visual retention and verbal function as well as deficits in concentration. Neither the character nor the degree of the neuropsychological deficits did depend on the affected vascular territory but on the existence of further cerebral infarcts on CT-scan.

Adult↗
PubMed1990

Epileptic seizures following ischaemic cerebral infarction. Clinical picture, CT findings and prognosis.

Clinical, CT and EEG findings of 100 consecutive patients suffering from epileptic seizures following hemispheric cerebral infarction were evaluated retrospectively. All patients were followed up for an average of 49 months. Twelve patients suffered from cardiogenic brain embolism, 20 had an occlusive disease of the internal cerebral artery. Forty-seven patients had a single middle cerebral artery infarct, 6 each a posterior cerebral artery or watershed infarct. CT showed lacunes in only 6 cases, 8 had multiple larger infarcts and 27 were normal. Seventy-six patients suffered from generalized seizures, 54 from partial fits, predominantly focal motor seizures. Seventy-one patients had their first seizure within the 1st year after stroke, 30 within 2 weeks after the infarct. The interval between stroke and the first epileptic fit exceeded 1 year in the remaining 29 cases. If the first fit occurred in the acute phase after stroke, the risk of further ones was significantly lower than when the first fit occurred in the chronic stage. The frequency of fits mainly depended on the occurrence of epileptic potentials in the EEG and the interval between stroke and the first seizure. During follow-up 27 patients suffered a recurrent stroke, and 52 patients died. Cardiac failure was the predominant cause of death; only 4 patients died as a consequence of an epileptic fit.

Aged↗
PubMed1989

[Multiple sclerosis and epilepsy. An analysis of 14 case histories].

Fourteen of 330 patients with the clinical and laboratory supported definite diagnosis of Multiple Sklerose (MS) had epileptic seizures. The epilepsy of six patients probably originates from the MS. Four patients respectively suffered from genuin epilepsy or symptomatic epilepsy caused by other diseases than the MS. Most patients had GM, two GM and focal motor fits and one uncinatus fits. An epileptic focus in the EEG was evident in two patients. MRI- and CCT-scans frequently showed extensive cortex-neighboured lesions and multiple subcortical demyelination, especially localized in the temporal lobe. Epileptic seizures as a symptom of MS are very seldom. The longer the interval from the first episode of the MS to the first epileptic seizure the more probable epilepsy is caused by other reasons than the MS.

Adult↗
PubMed1988

[Viral encephalitis. Experiences with 53 patients in Middle Hessia].

Clinical symptoms, course of disease, cerebrospinal fluid (CSF) and cranial CT of 53 patients suffering from acute or subacute encephalitis were evaluated retrospectively. The virus could be identified in 21 (39%) patients. Nine of them had herpes simplex virus-encephalitis. 16 patients, eight with herpes simplex virus-encephalitis, died due to the disease. Complete restitution could be observed in 73% of survivors. Disturbance of consciousness and severe focal neurological deficit worsened prognosis towards letality and functional recovery. Most patients had initially elevated number of cellular elements and/or pathological protein concentration in CSF. CSF protein profile showed disturbance of blood-CSF-barrier function in a great number of patients during the first week of the disease whereas autochthonous production of immunoglobulin G was observed predominantly during the second and third week. Elevated concentration of CSF-lactate was seen in herpes simplex virus-encephalitis and in letal cases. 28 (53%) patients had pathological CT-findings. Generalized brain edema, focal hypodensities, focal and cortical contrast enhancement and hemorrhagic imbibation were observed. With one exception patients with herpes simplex virus-encephalitis had hypodense lesions in the temporal lobe. Besides this CT-findings did not allow conclusions regarding the etiology of encephalitis. Prognosis of encephalitis caused by other than herpes simplex virus was worse in case of pathological CT.

Acquired Immunodeficiency Syndrome↗
PubMed1987

[Fatal outcome of ischemic cerebral infarct].

During 1977 to 1985 2008 patients suffering from acute ischemic cerebral infarcts were admitted to the Department of Neurology, Giessen University. 213 (10.6%) died during their stay at hospital of 28 days in average. Time of survival, cause of death, localization and etiology of the infarcts were evaluated retrospectively on base of the medical reports, the angiographic, doppler-sonographic, computerized tomographic, and autopsy findings. The same number of patients died because of direct sequelae of stroke and secondary complications respectively. Those with supratentorial infarcts, who died in consequence of a vegetative dysregulation generally did not survive the first week after ictus, often had infarcts exceeding the supply area of one large cerebral artery and frequently had evidence of cardiac embolism. Pathogenetic factors for extension of the ischemic cerebral damage subsequently causing transtentorial herniation were spreading thrombosis, reinfarction, and fatal secondary hemorrhage. Patients dying in consequence of an infratentorial infarct often had a thrombosis of the basilar artery or a large cerebellar infarction. Secondary fatal complications mostly occurred after the first week after stroke. Pulmonary edema, pulmonary embolism and myocardial infarction predominated with different time pattern.

Adult↗
PubMed1986

CSF cyclic AMP and CSF adenylate kinase in cerebral ischaemic infarction.

The severity of neurological deficits, size of hypodense zone on CT, concentration of cAMP and activity of adenylate kinase in cerebrospinal fluid (CSF) were evaluated at predefined intervals in the acute stage of supratentorial cerebral ischaemic infarction in 52 patients. Patients with cerebral infarction had raised activities of adenylate kinase CSF as compared with normal persons. Patients with marked neurological deficits, only slight improvement of neurological signs and large infarction zones on CT had higher average activities of adenylate kinase and lower concentration of cAMP in CSF. Alterations of CSF adenylate kinase and CSF cAMP values were most distinct on the 3rd day after the stroke. Reasons for the changes may be metabolic disorders following brain ischaemia.

Adenylyl Cyclases↗
PubMed1984

[Prognostic criteria on the cranial computed tomogram of an ischemic cerebral infarct].

Two hundred and eighty-three cranial computer tomograms in 214 patients with supratentorial ischaemic infarcts were analysed with reference to the prognosis. Patients with large infarcts often have a poor prognosis. Contrast accumulation indicates a poor prognosis only in the first week. Enhancement in the second and third week was more common and more intense. Diapedesis from necrotic capillaries is thought to be responsible for early enhancement and increased pinocytosis in regenerated endothelium for late enhancement.

Cerebral Infarction↗
PubMedDate not supplied

Intravenously administered acetylsalicylic acid in combination with low-dose heparin in acute ischemic stroke: a safety analysis.

Although therapy with acetylsalicylic acid (aspirin, ASA) is well established in secondary prevention of stroke, efficacy and side effects of this substance in acute stroke treatment are undetermined. ASA may be useful in acute cerebral ischemia because of its potential to prevent thrombus propagation and neuronal damage. A total of 268 patients with an acute cerebral ischemia, who were admitted to our stroke unit within 24 hours after stroke, were treated with intravenously administered ASA (0.5 g/day) in combination with low-dose heparin. The functional status of the patients was assessed after 1 month using the modified Rankin Scale. Eighteen (6.7%) patients died during the observation period. The functional status according to Rankin Scale was classified as stage 0 in 76 (28.3%), 1 in 59 (22.0%), 2 in 39 (14.6%), 3 in 32 (12.3%), 4 in 36 (13.4%), and 5 in 7 (2.6%) patients. A symptomatic secondary intracerebral hemorrhage was seen in one patient. Gastrointestinal symptoms were observed in 13 (4.8%) patients, including five instances of gastrointestinal bleeding. Further complications were allergic reactions to aspirin (one) and hematuria (one). Recurrent cerebral ischemia occurred in nine (3.3%) patients (five with transient ischemic attack or minor stroke) during the observation period. We conclude that treatment of acute ischemic stroke with intravenously applied aspirin in combination with low-dose heparin is safe. Efficacy of this therapy should be elucidated in a controlled trial.

Acute Disease↗