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Biomedical subjects

F Aichner

Publications and source records attributed to F Aichner.

At least 55 records · Page 3Linked to original sources

Imaging of inner cerebral trauma.

The concept of "Inner cerebral trauma" (ICT) has been preliminary defined as a characteristic topographic pattern of deep brain lesions produced by physical forces occurring within the cranial cavity in closed head injury of the acceleration/deceleration type. The lesions, based on neuropathological examinations, are characteristically localized in the "centro-axial" regions of the brain. The extent of ICT is often underestimated by CT. Due to assess the value of MR imaging, 83 patients with ICT were examined on a 1.5 T unit in different stages after trauma. The pattern of lesions, as shown with MR imaging, correlated well with neuropathological studies, suggesting a multifocal pathogenesis of severe traumatic brain injury.

Adolescent↗

[Neurologic manifestations of diabetes mellitus: an overview].

Neurological manifestations of diabetes mellitus comprise structural changes in both central and peripheral nervous system, as well as functional cerebral disturbances. Macro- and microangiopathy are responsible for the development of cerebrovascular diseases; microangiopathic and metabolic disturbances are considered in the discussion to be responsible for the development of the various forms of diabetic polyneuropathy. Acute metabolic episodes with progressive impairment of consciousness have to be differentiated from structural neurological disorders. As a further point of interest the association between diabetes mellitus and special neurological diseases is mentioned.

Brain Diseases, Metabolic↗

Sneddon's syndrome. A long-term follow-up of 21 patients.

BACKGROUND AND DESIGN: Twenty-one patients with histologically proven Sneddon's syndrome were followed up in a retrospective study. We report on their detailed clinical courses and extensive follow-up examinations. RESULTS: Incidence is estimated at four cases per million population per year. Nonspecific prodromal symptoms (headache, dizziness) frequently (80%) precede livedo racemosa for 3.5 and (multi)focal neurological symptoms of fully developed disease for 9 years followed by progressive cognitive impairment (60%) 10 years later. Involvement of fundi, peripheral nerves, heart, and kidneys is frequent (50% to 70%) yet usually asymptomatic. Some symptoms prove irreversible (livedo racemosa, multifocal cerebral lesions on imaging, or creatinine clearance), whereas other symptoms tend to resolve after days to years (many focal neurological symptoms, some electrocardiographic changes, or hypertension). Mortality is calculated at 9.5% within an average observation time of 6.2 years. Laboratory findings, including antiphospholipid antibodies, are normal except for elevated erythrocyte sedimentation rates and complement consumption at times of disease progression and increased cholesterol levels parallel to disease extent. Skin biopsy specimens reveal inflammatory findings ("endothelitis") of small- to medium-sized arteries followed by subendothelial proliferation and fibrosis. Hypertension is the only risk factor significantly associated with a more severe course of the disease; no medication proved effective. CONCLUSIONS: Sneddon's syndrome is an often unrecognized, slowly progressive, systemic disease with evidence of vasculitic origin.

Adult↗

Early detection of post-traumatic olivary hypertrophy by MRI.

Two patients are described, in whom MRI detected unilateral signal abnormalities in the region of the inferior olivary nuclei, suggesting an early stage of olivary hypertrophy. MRI was performed 4 and 7 weeks respectively after traumatic brain-stem injury. Palatal myoclonus was concomitantly observed in one patient, while the other showed no evidence of segmental myoclonus at the time of examination. The authors conclude that MRI is highly sensitive in the detection of olivary hypertrophy and of traumatic lesions of the dentato-rubro-olivary pathway.

Adult↗

Post-traumatic segmental myoclonus associated with bilateral olivary hypertrophy.

We present clinical and magnetic resonance (MR) findings in three patients with segmental myoclonia occurring 11-18 months after severe brainstem injury. Palatal myoclonus and vertical ocular myorhythmia were present in all three patients and synchronous involuntary movements of the upper extremities ("wing beating") in two patients. MR-imaging showed multiple post-traumatic lesions within the dentato-rubro-olivary pathway ("myoclonic triangle"), associated with bilateral enlargement and increased signal intensity of the inferior olives. The signal abnormality was more prominent on proton density weighted images than on T2-weighted images, suggesting underlying pathological changes different from typical gliosis.

Adolescent↗

[Trans-septo-sphenoidal operation for pituitary adenoma in 92 patients: results and follow-up endocrine studies].

The short- and long-term therapeutic results of transseptosphenoidal adenomectomy were studied retrospectively in 92 patients with pituitary tumors (42 nonsecreting adenomas, 21 GH-, 15 PRL-, 10 ACTH-, 2 TSH-, and 2 FSH-secreting adenomas). Severe surgically related complications were not observed. The early remission rate was 53.7% in nonsecreting, 57.1% in GH-secreting, 60% in PRL-secreting, 88.9% in ACTH-secreting, and 75% in TSH- or FSH-secreting adenomas. The recurrence rate in patients with nonsecreting adenomas was 47.1%, with GH-secreting adenomas 10%, with ACTH-secreting adenomas 25%, and with TSH- or FSH-secreting adenomas 66.7%, respectively. A long-term cure rate of 69.2% was observed in prolactinomas in combination with a facultative dopamine agonist therapy. More patients had normal pituitary function concerning TSH, ACTH, and LH/FSH post-operatively (48.9% versus 46.6% preoperatively). These data confirm that transseptosphenoidal surgery is a safe and selective treatment for pituitary adenomas with efficient preservation of the normal pituitary gland.

Adenoma↗

[Cerebellar atrophy and phenytoin poisoning. An MR study].

Phenytoin has been considered a possible cause of cerebellar degeneration, especially after clinical intoxication. Magnetic resonance provides the diagnosis of anatomical structures in the posterior fossa without the limitation of beam hardening artefacts. The aim of this study was to evaluate the relationship of phenytoin medication and cerebellar atrophy in 11 patients with increased serum levels (21.4 micrograms/ml-95.6 micrograms/ml). Five patients had normal cerebellar structures, although three of them had a history of clinical intoxication and all had at least one episode of increased serum level of DPH. The remaining six patients had moderate severe cerebellar atrophy (n = 4) and atrophy of the vermis cerebelli (n = 5). Two of them had never experienced clinical intoxication. There was no correlation between the degree of atrophy and severity of clinical symptoms and evaluation of serum DPH levels (up to four times normal values). There was also no correlation between cerebellar atrophy, duration of epilepsy and frequency of seizures. We conclude that phenytoin overdosage does not necessarily result in cerebellar atrophy and it is unlikely that phenytoin medication was the only cause of cerebellar atrophy in the remaining patients.

Adult↗

Magnetic resonance: a noninvasive approach to metabolism, circulation, and morphology in human brain death.

Phosphorus (31P) magnetic resonance spectroscopy and magnetic resonance imaging were used to study the intracellular metabolism, circulation, and morphology in the brains of 3 patients with clinical brain death syndrome due to traumatic brain damage, subarachnoid hemorrhage, and acute occlusive hydrocephalus caused by a colloid cyst. Magnetic resonance spectra were characterized by a complete absence of ATP and were dominated by an intense inorganic phosphate signal. Magnetic resonance imaging revealed a uniform pattern of diffuse brain swelling and tentorial and foraminal herniation. Intracranial blood flow was absent on the magnetic resonance angiography projections. These preliminary findings suggest an important impact of magnetic resonance in the determination of human brain death.

Adenosine Triphosphate↗

Magnetic resonance imaging and angiography in hemifacial spasm.

We used magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) to investigate 14 patients with unilateral hemifacial spasm (HS) and 20 controls. The relationship of the seventh and eighth cranial nerves to adjacent vessels was best visualized on the contiguous flow sensitive 3D-FISP images. Reconstruction of projectional MRA was helpful to assess the complex architecture of the vertebrobasilar system. Neurovascular contact in the facial nerve root exit zone was present in 4 of 20 controls and in 12 of 14 patients, in whom it predicted the affected side. These results support previous findings of surgical and electrophysiological investigations that local irritation of the facial nerve is the most possible explanation for HS. MRI and MRA provide vascular and brain tissue diagnosis in a single non-invasive examination and should be recommended as primary neuroradiological procedure in HS.

Aged↗

Electrophysiological findings in a case of severe intrathecal baclofen overdose.

Multimodality evoked potentials were examined in a case of serious accidental intrathecal baclofen overdose in a patient who suffered from severe spasticity due to a traumatic brain lesion. Electrophysiological findings during, before and after the intoxication were compared. Transcranial electrical stimulation up to 750 V did not evoke any responses in thenar muscles on the first day of intoxication. An improvement to normal values was observed within 3 days, paralleled by an amelioration of the patient's clinical condition. Cervical electrical stimulation was largely unaffected by baclofen. Median nerve somatosensory and brain-stem acoustic evoked potentials revealed few or no differences during intoxication compared to pre- and post-intoxication responses.

Adolescent↗

Superficial siderosis of the central nervous system: report of three cases and review of the literature.

We present 3 cases and a review of the literature to demonstrate the current state of clinical diagnosis and therapy of superficial siderosis of the central nervous system. Typical symptoms were progressive cerebellar ataxia, spasticity and hearing loss. Repeated subarachnoid hemorrhage was indicated by persistent xanthochromia of the cerebrospinal fluid and confirmed by the presence of erythrophages, siderophages and iron-containing pigments. Deposition of free iron and hemosiderin in pial and subpial structures leads to intoxication of the central nervous system and represents the pathophysiological mechanism of superficial siderosis. Hypointensity of the marginal zones of the central nervous system on T2 weighted MR images indicates an iron-induced susceptibility effect and seems pathognomonic for superficial siderosis. In 39 of the 43 previously described cases superficial siderosis was verified by biopsy or autopsy. Today magnetic resonance imaging enables diagnosis at an early stage of the disease. Therapeutic management requires the elimination of any potential source of bleeding. In patients with unknown etiology no proofed therapy is yet available.

Aged↗

1-H-localized magnetic resonance spectroscopy: preliminary observations in transient ischemic attacks.

Water-suppressed proton magnetic resonance spectroscopy which has recently shown diagnostic potential in human stroke victims was performed in two patients who had suffered a hemispheric transient ischemic attack. Localized spectra were targeted from routine MR images. In one patient lactate could be observed 8 weeks after a transient ischemic attack. Lactate concentration was low compared with that of a patient who had suffered acute stroke. The other TIA patient did not show evidence of lactate production. Although these observations are preliminary, we demonstrated that localized in vivo proton spectroscopy can detect persistent biochemical alterations after transient ischemic attacks. We suggest that non-invasive in vivo proton spectroscopy will become a useful method in diagnosis and management of TIA in the future.

Aged↗

[Wilson's disease with primary CNS manifestation--current status in diagnosis and therapy].

Five cases studied at our clinic are discussed and the literature reviewed with the aim of assessing the diagnostic value of various examination methods used for Wilson's disease and a modified diagnostic approach is suggested. CT and MRI are compared with regard to sensitivity, specificity and prognostic value. Almost regularly, MRI showed bilateral lesions in the basal ganglia in combination with structural changes in the brain stem. A pattern consisting of symmetrical lesions of the red nuclei, the periaqueductal grey region and, facultatively, the substantia nigra and the dentate nuclei was discovered and appeared almost pathognomonic. Follow-up studies revealed excellent reversibility of MRI changes by both penicillamine and trientine. Auditory evoked potentials showed the highest sensitivity and the best correlation with structural findings. Kayser-Fleischer corneal rings--a diagnostic requirement in the literature--were not found in all patients. The current state of therapy and therapy management is discussed on the basis of pathophysiological considerations. As possible complications of penicillamine administration the deterioration of the clinical condition after initiating therapy, and the risks associated with an abrupt termination of therapy are discussed in detail.

Adolescent↗

Septo-optic dysplasia and growth hormone deficiency: accelerated pubertal maturation during GH therapy.

We report four patients (three male, one female) with septo-optic dysplasia and growth hormone deficiency. All had GH therapy for a period of four to eight years until reaching final height. In all four cases bone maturation during puberty was accelerated (1.4 to 1.9 "years"/year), resulting in a final height which was clearly below the predicted height. The progress of pubertal stages was very short in all patients. In three patients TSH and prolactin release after TRH stimulation were increased. These data support a hypothalamic original of the endocrine disorder. Insufficient GH release, even after repeated GHRH stimulation, is in contrast to this assumption. In one case there was a late manifestation of neurohormonal diabetes insipidus, which indicates the possibility of later disease progression. MR imaging of the brain demonstrated variable malformation of the septum pellucidum, chiasma and nervus opticus or the pituitary gland, respectively.

Abnormalities, Multiple↗